The Triage Health Trajectory Tool is designed to show you something most people never see until it’s too late: what your health metrics will look like 20, 30, or even 50 years from now. The thing is, your body doesn’t just suddenly fall apart one day. Conditions like diabetes, heart disease, and sarcopenia develop slowly, through thousands of small decisions compounded over decades. That may seem grim, but it’s actually the good news, because it means you have time to change the trajectory.

The Triage Health Trajectory Tool takes your current health metrics (things like your cholesterol levels, blood pressure, VO₂ max, body composition, and strength markers) and projects them forward across your lifespan. But it doesn’t just show you one future. It shows you three.

  1. Natural Decline: What happens if you continue with a sedentary modern lifestyle. We’re talking VO₂ max dropping by 50%+, strength losses of 50-85%, metabolic markers sliding into pre-diabetic ranges, and body fat creeping up year after year.
  2. Maintenance: What you can achieve with basic, consistent effort: exercising a couple of times per week, eating a decent diet, getting 7-8 hours of sleep, managing stress reasonably well. This typically slows decline by about 50% compared to doing nothing.
  3. Optimisation: What’s possible when you really dial things in: training 4-6 times per week with a structured program, nutrition dialled in for your goals, excellent sleep hygiene, and consistent stress management (potentially along with other interventions). This can often not just slow decline, but actually reverse it for years or even decades.

I know it is hard to really visualise this across your lifespan, which is why I created this tool. The main thing that prompted me to create this was that, having worked with hundreds of clients over the years, I noticed that the ones who succeed long-term understand the compound effect. They get that lifting weights today isn’t just about looking good next month, it’s about being able to pick up their grandkids in 30 years. Managing blood sugar now isn’t just about fitting into jeans; it’s about avoiding dialysis when they’re 70. These results are invisible right now, but that doesn’t make them unimportant.

This tool makes the invisible visible. You’ll see exactly when your VO₂ max might drop into the high-mortality-risk zone (given population averages). When your strength might decline to the point where getting off the floor becomes difficult. When your metabolic markers might cross into pre-diabetic territory.

But more importantly, you’ll see how different choices lead to radically different outcomes. The 35-year-old who starts optimising now can maintain the fitness and metabolic health of someone 20-30 years younger. But it’s also important to realise that it’s never too late to start, and even maintenance-level efforts at any age provide meaningful benefits.

Before we dive in, I do just want to note that these are projections based on population averages and scientific studies, and are not prophecies. Your individual results will vary based on genetics, health history, environmental factors, and dozens of other variables. Think of the Triage Health Trajectory Tool more like a financial compound interest calculator that is based on the stock market. It shows you likely outcomes based on different “investment strategies” for your health, but actual returns depend on consistent execution and individual factors. You wouldn’t invest without seeing some sort of projected return on investment, and historical analysis, but that is what you are doing with your health by not seeing the trend. 

Now, I don’t claim to have a crystal ball, and these are just best guesses based on population averages, but the general patterns are solid. The science is clear that inactivity, poor nutrition, and lifestyle factors drive a lot of the decline. I can tell you this from my own life, as some of my younger brothers have grey hair, while I have none. Genetics play a role, but lifestyle also plays a pretty big role. Movement, proper nutrition, sleep, and stress management often slow or reverse the decline. The specific numbers might vary for you personally, based on your genetics and situation, but the direction is undeniable.

Now, before we get into using the Triage Health Trajectory Tool and looking at all the numbers, I need to be honest with you about something: your brain is working against you on this.

For 200,000 years of human evolution, your ancestors lived in environments where immediate threats mattered and long-term planning beyond the next season was largely irrelevant. A hungry predator today was evolutionarily significant. Heart disease in 40 years? That’s a modern invention that your Paleolithic brain simply isn’t wired to process.

Behavioural economists call this “temporal discounting” or “hyperbolic discounting”, which is where we dramatically undervalue future outcomes compared to immediate ones. You’d rather have €100 today than €200 next year, even though waiting is objectively better. You’d rather skip the gym today (immediate comfort) than maintain excellent VO₂ max at age 75 (distant, abstract benefit).

This tool is designed to fight that cognitive architecture. It takes the invisible and distant (“I would like to be healthy at 80”) and makes it visible and concrete (“Your VO₂ max will be 21 ml/kg/min at age 80, putting you in the Very Poor range with 5x mortality risk”).

What psychologists call “construal level theory” helps explain that we think about near events concretely and distant events abstractly. The problem is that all the consequences of your health choices are distant events… until suddenly they’re not, and by then it’s often too late.

So if you find yourself looking at these projections and still struggling to change behaviour, that’s not a character flaw. That’s 200,000 years of evolution telling you to prioritise the immediate over the distant. The key question is: are you going to let your Paleolithic brain determine your 21st-century outcomes?

Alright now, let’s get stuck into actually using the Triage Health Trajectory Tool. You will need to gather the same information you need for our Ultimate Health Targets Assessment tool, and these two tools work synergistically together.

 

Triage Health Trajectory Tool

Triage Health Trajectory Calculator

See a glimpse of your health metrics 20, 40, even 60 years into the future

💡 Visualise how today's choices compound across your entire lifespan

Basic Information

💡 Choose how many years into the future to project (capped at age 100)

Unit System

💡 Note: Enter values in your preferred units. Charts and projections will display in metric (standard for scientific analysis).

📊 Current Health Metrics

Enter your current values for the metrics you want to track over time. Leave blank any you don't have.

Cardiovascular Markers

Metabolic Markers

Inflammatory & Kidney Markers

Fitness Markers

Strength (Optional)

💡 Tip: Enter your bodyweight above to calculate strength ratios (×BW)

Body Composition

💡 Tip: Enter height + weight for BMI trajectory
+ body fat % for FFMI (Fat-Free Mass Index) trajectory

Recovery & Sleep

Hormones

How This Works

This calculator projects three possible futures for health:

  • Natural Decline - This shows the typical age-related deterioration. If you make no changes to your current lifestyle (assuming you live the avergae lifestyle.
  • Maintenance - This shows what you can do with minimal effort (2-3x/week exercise, basic dietary awareness). Typically, this can slow decline by ~50%.
  • Optimisation - This shows what can realistically be accomplished with dedicated effort (4-6x/week structured training, nutrition optimisation), and can often lead to prevention or the reversal of decline. Of course, this is just an estimation, and your results may vary. I have seen people make drastic changes to their markers, and others make smaller changes, with the same interventions. So, results do vary.

Key Insights:

  • This allows you to see how small daily choices do actually compound over decades.
  • It can also help you to identify when you'll cross critical health thresholds (estimated).
  • It can also help you to calculate/estimate the extra years of healthy, independent living you will be able to get with health optimisation.

💡 The Compound Effect

You really should not ignore the compound effect with this stuff. For example, a 30-year-old with VO₂ max of 45 ml/kg/min:

  • Natural: Their VO₂ max drops to ~20 by age 80. This likely leads to poor health, and a high mortality risk.
  • Optimisation: Whereas if they spend some time optimising things, they are able to maintain a VO₂ max of ~43 by age 80, which is effectively the health of a 50-year-old!

Result: By spending some time optimising, they are able to get ~8-12 extra years of life expectancy, plus decades more of vitality and independence.

Important Notes

  • These projections are based on population averages and scientific studies. This is not medical advice, and it is not guaranteed.
  • Individual results vary based on genetics, environment, the exact protocols use, and adherence.
  • Starting intervention at ANY age provides benefits. The best time to start was 20 years ago. The second best time is now.
  • We highly recommend that you consult your healthcare provider(s) before making major lifestyle changes.

 

Understanding Your Triage Health Trajectory Tool Results

Alright, so you’ve entered your data and hit that calculate button. Now you’re staring at a bunch of charts, numbers, and coloured bands, probably thinking, “what am I actually looking at here?” Let me break it down for you, because understanding how to read these results is crucial to getting value from the tool.

 

The Three Lines: Your Possible Futures

The most obvious thing you’ll see is the chart with three coloured lines stretching across your lifespan:

The red line (Natural Decline): This is your “do nothing” trajectory. It assumes you continue living like the average sedentary modern adult: minimal exercise, typical Western diet, inadequate sleep, poor stress management. I’m not going to lie to you, this line is usually pretty depressing to look at. But that’s intentional. This is what happens when you let biology and modern life have their way with you without putting up a fight.

The orange line (Maintenance): This is your “basic effort” trajectory. We’re talking about hitting the minimum exercise guidelines (150 minutes of moderate intensity cardio per week and at least 2 resistance training sessions, working the whole body), eating a reasonably healthy diet most of the time, getting decent sleep, and managing stress somewhat effectively. Nothing heroic, nothing extreme, just consistent, sensible health behaviours. You’ll notice this line is significantly better than the natural decline line. That’s the power of just showing up regularly.

The green line (Optimisation): This is your “fully dialled in” trajectory. Training 4-6 times per week with a proper program, nutrition optimised for your goals, sleep and recovery prioritised, and stress managed proactively. This is what’s possible when you treat your health like a serious priority. You’ll often see this line actually improve for the first few years before eventually declining much more slowly than the other two.

 

The Coloured Bands: Your Health Zones

Now, look at the background of the chart. You’ll see horizontal bands in different colours: green, yellow, orange, red, and dark red. These represent different health ranges for whatever metric you’re looking at:

Green (Optimal): This is where you want to be. Values in this range are associated with the lowest disease risk and best health outcomes. This is peak performance territory.

Yellow (Good): Still pretty solid. You’re doing well, not at serious risk, but there’s room for improvement if you want to optimise further.

Orange (Average): This is “normal” for the general population, which unfortunately doesn’t mean it’s good. Average, in modern society, often means “on the path to chronic disease, just not there yet.” Being average is not something to celebrate when the average person is unhealthy.

Red (Poor): Now we’re in concerning territory. Values here are associated with significantly elevated disease risk. This is where you start seeing real health consequences.

Dark Red (Very Poor): Danger zone. These values indicate serious health problems or very high risk of developing them soon. Medical intervention is often necessary at this level.

 

What You’re Actually Tracking

As you click through different metrics in the calculator, you’re seeing how each one evolves over time. Let me give you a framework for thinking about what these different metrics tell you:

Cardiovascular markers (ApoB, LDL, triglycerides, HDL, blood pressure): These tell you about your heart disease and stroke risk. They’re hugely influenced by diet, exercise, body composition, and genetics. The scary thing is that they tend to worsen significantly with age in sedentary populations, which is why heart disease is the leading cause of death in developed countries.

Metabolic markers (fasting glucose, HbA1c, liver enzymes): These show you how your body handles sugar and whether you’re headed toward metabolic syndrome, prediabetes, or type 2 diabetes. In the natural decline scenario, you’ll often see these markers sliding into pre-diabetic territory by age 60-70. That’s not inevitable; it’s the accumulation of small choices.

Fitness markers (VO₂ max, resting heart rate, HRV): These are your “functional capacity” indicators. VO₂ max, in particular, is one of the strongest predictors of longevity we have. When you see the natural decline line for VO₂ max dropping by 50%+ over 50 years, you’re looking at the difference between being vibrant and independent at 80 versus being frail and struggling with basic activities.

Strength markers (squat, deadlift, bench press, chin-ups): These show your muscular capacity and, to some extent, your resistance to sarcopenia (age-related muscle loss). The natural decline trajectory for strength is brutal; we’re talking about 50-85% losses by age 80. That’s the difference between climbing stairs easily and needing a walker.

Body composition markers (body fat %, waist circumference, BMI, FFMI): These track how your body composition changes over time. The natural trajectory is gaining fat and losing muscle simultaneously, which is the worst possible combination. The optimisation trajectory often shows you can actually improve body composition well into middle age and beyond.

 

The Summary Stats: Your Bottom Line

Below the chart, you’ll see three cards showing where each trajectory ends up by your target age:

  • The final value: This is what the metric will be at the end of your projection period
  • The health range: This tells you which coloured band you’ll be in (Optimal, Good, Average, Poor, or Very Poor)
  • When you cross into poor territory: If applicable, this shows you the age at which that trajectory drops you into the Poor or Very Poor range

Pay close attention to these. They’re your “bottom line” numbers. For example, if your Natural Decline VO₂ max ends up at 21 ml/kg/min (Very Poor) but your Optimisation trajectory keeps you at 43 ml/kg/min (Good), that’s the difference between high mortality risk and excellent health span.

 

The Insights Section: What It All Means

Scroll down further and you’ll see the Key Insights section. This is where the calculator does some analysis for you and highlights the most important findings:

Critical insights (marked in red): These are the big deals. Metrics where optimisation makes a massive difference in your outcome, or where natural decline leads you into seriously problematic territory.

Warning insights (marked in orange): These are notable benefits of optimisation, but perhaps not as dramatic as the critical ones. Still worth paying attention to.

Info insights (marked in blue): These are interesting observations about your trajectory that might not be critical but are worth knowing.

The calculator looks at things like: How many health bands does optimisation move you across? How many years does it delay you from entering poor ranges? What’s the percentage difference between natural decline and optimisation outcomes?

 

The Band Transitions Section: Your Timeline

This section shows you when you transition between different health ranges. For example, you might see:

  • Age 35: Optimal
  • Age 52: Drops to Good (Natural Decline)
  • Age 61: Drops to Average (Natural Decline)
  • Never drops below Good (Optimisation)

This timeline perspective is incredibly valuable because it shows you when things start to go wrong if you don’t intervene, and how much time optimisation buys you in the good ranges.

 

How to Actually Use These Results

Here’s what I want you to do with all this information, keeping in mind that I am not a doctor, and you should be consulting an actual medical professional about all of this stuff:

First, don’t panic if your natural decline trajectory looks grim. That’s the point, it’s showing you what happens if you change nothing. The good news is that you can change things.

Second, focus on the metrics where there’s the biggest gap between natural decline and optimisation. Those are your highest-leverage opportunities. If optimisation keeps your VO₂ max 20+ points higher than natural decline, cardiovascular training should be a priority for you.

Third, look for patterns across multiple metrics. If several metabolic markers are trending poorly, that’s telling you something about your diet and body composition. If strength markers are declining rapidly, you need to prioritise resistance training.

Fourth, use the band crossing timeline to set concrete goals. If the calculator shows you’ll drop into the Poor range for a metric at age 55 with natural decline, but stay in Good range with optimisation, you now have a clear “why” for putting in the work.

Finally, remember that these trajectories aren’t destiny; they’re forecasts based on different behaviour patterns. You can switch trajectories at any point. Starting optimisation at 50 is better than never starting at all.

The Triage Health Trajectory Tool isn’t here to judge you or make you feel bad about where you’re at. It’s here to show you, in concrete terms, what your choices compound into over decades, because once you see that your decision to train today or skip it, to eat well or grab fast food, isn’t just about today, it’s about which of these three trajectories you’re choosing, those decisions become a lot easier to make.

Now, I think it is important to talk about the assumptions and limitations built into these projections, because understanding those is crucial to interpreting your results correctly.

 

Epistemic Humility

Alright, before we go any further, I need to be frank with you about what this tool is and what it isn’t. Because the last thing I want is for you to treat these projections as gospel truth or, conversely, to dismiss them entirely because they’re not perfectly precise. Neither extreme is helpful.

 

You Are Not a Population Average

Here’s the fundamental limitation of any health calculator, including this one: it’s built on population averages and scientific studies, but you are an individual.

What does that mean in practice? Well, let’s say the research shows that sedentary adults experience a 1% decline in VO₂ max per year after age 35. That’s a solid, well-established finding backed by decades of data. But here’s what it doesn’t tell you: whether you specifically will decline at 0.8% per year or 1.2% per year. Maybe you have exceptional cardiovascular genetics. Maybe you have a polymorphism that affects your mitochondrial function. Maybe you live at altitude, or you have a job that keeps you more active than the average desk worker, or you have a health condition that wasn’t factored into the studies.

The projections in this tool represent what happens to the typical person in each scenario. But “typical” is a statistical construct, not a real human being. Some of you will respond dramatically better to training and nutrition interventions than these projections suggest. Others will find certain metrics harder to move, no matter how dialled in you are.

I’ve had clients who started with a VO₂ max of 35 ml/kg/min at age 45 and got it up to 55 within two years through dedicated training. That’s way better than the optimisation trajectory would predict. I’ve also had clients who did everything “right” and saw more modest improvements. Genetics matter. Training history matters. Sleep quality matters. Stress levels matter. Along with dozens of other factors I can’t possibly account for in a simple tool like this (I mean, if someone wants to pay me a couple of million to try and create something that does take all of these into account, I am game).

So when you see your optimisation trajectory showing a 15% improvement in a metric over two years, understand that’s the typical response. You might see 25%. You might see 8%. Both are normal.

 

Genetic Ceilings and True Non-Responders

Unfortunately, even among people who execute the optimisation lifestyle perfectly for decades, there’s massive individual variation in how specific metrics respond.

The trajectories shown here are built on population averages, often from studies of health-conscious individuals or masters athletes. They represent what’s realistically achievable for a large portion of the population. But they’re not a guarantee for you personally on every single metric.

Let me give you some very rough data on true non-responders:

Research has found that roughly 15-20% of people are almost complete non-responders to aerobic training for HDL-C and triglyceride improvement. ~5-10% are non-responders for VO₂ max gains, even with consistent, properly-structured cardio training. At the other extreme, some people get 2-3x the average improvement from the same training program

For strength and muscle mass, roughly ~10-15% of people are “low responders” even on perfect progressive-overload programs with high protein intake.

Lipid responses show enormous variation. Some people drop ApoB/LDL by 50% from dietary changes alone. Others barely move the needle and need medication to achieve meaningful improvements. This isn’t about effort; it’s about genetic differences in cholesterol absorption, synthesis, and clearance.

Testosterone response to lifestyle optimisation varies wildly in men. Some see increases of 200-300 ng/dL from sleep optimisation, weight loss, and training. Others plateau quickly because of SHBG polymorphisms, Leydig cell sensitivity variations, aromatase activity or any other number of issues that you can’t exactly control for. The same lifestyle interventions produce dramatically different hormonal responses.

This is not an excuse. This is just biology.

Your genetic “ceiling” for a particular trait may be lower (or higher!) than the optimisation trajectory suggests. A small percentage of people will follow optimisation protocols to the letter and still end up with merely “average” numbers in one or two metrics by age 70.

But the critical insight is that almost nobody is a non-responder to everything. The same person who gets zero HDL improvement from cardio often gets massive strength and body-composition improvements from resistance training. The person who barely moves the needle on VO₂ max might see dramatic improvements in metabolic markers, inflammation, and body composition. The non-responder rate to the overall lifestyle package (measured by all-cause mortality, healthspan, physical function, and quality of life) approaches zero. The benefits are simply distributed across different systems in different people.

Some people’s optimisation shows up primarily in cardiovascular metrics. Others see it in metabolic health. Others in strength and body composition. Others in inflammation and longevity markers. But almost everyone who optimises consistently sees major improvements somewhere.

So, how do you use this information:

First, treat the optimisation trajectory as the population-average best-case, not your personal promise for every single metric. You might exceed it in some areas and fall short in others. That’s normal.

Second, test, intervene, retest. This is how you discover where you’re a high responder and where you’re not. If six months of legitimate Zone 2 training plus HIIT doesn’t move your VO₂ max or HDL at all, you’re probably in that 10-15% tail for that specific adaptation. That’s valuable information. Shift focus to the dozens of other levers that do work for you.

Third, do not use “I might be a non-responder” as a pre-emptive excuse before you’ve actually tried. Most self-labelled non-responders are simply under-dosed (too little volume, intensity, or consistency) or have undetected confounders like sleep apnea, subclinical hypothyroidism, undiagnosed food sensitivities, or chronic stress that’s blocking adaptation.

Give legitimate optimisation a real shot (6-12 months of consistent, properly-executed intervention) before concluding you’re a non-responder. And even if you are a non-responder for one metric, you’re almost certainly a responder for others.

The bottom line is that the optimisation trajectory is still the highest-expectation play by orders of magnitude, even after factoring in genetic variation. Yes, there’s individual variability. Yes, you might not hit the green line on every metric. But the natural decline trajectory is almost never anyone’s genetic ceiling. That’s what happens when you do nothing and let modern life have its dirty way with you.

Your genetics determine where your ceiling is. Your choices determine whether you get anywhere close to it. Don’t use genetic variation as an excuse to not try. Use it as a framework to understand your individual response pattern, double down on what works for you, and accept that not every metric will be optimal, and that’s okay. The compound effect across all the metrics you do improve is still massive.

 

This Is About Making The Invisible Visible

The real value of this tool isn’t in predicting your exact cholesterol level at age 67 down to the decimal point. That’s impossible, and anyone who claims otherwise is selling you snake oil. The value is in making long-term trajectories visible and concrete.

Most people live their lives completely disconnected from the long-term consequences of their daily choices. They know, abstractly, that “exercise is good for you” and “you should eat vegetables.” But that knowledge doesn’t translate into behaviour change because it’s too vague, too abstract, too distant.

What does “good for you” actually mean? How good? Good in what way? By how much? When?

The Triage Health Trajectory Tool attempts to answer those questions in concrete terms. It shows you that your choice to train consistently doesn’t just make you feel a bit better; it potentially keeps your VO₂ max 20+ points higher three decades from now. It shows you that optimising your nutrition doesn’t just help you lose a few pounds; it might keep your HbA1c in the optimal range instead of crossing into diabetic territory in your 60s.

It makes the invisible visible. It makes the abstract concrete. It makes the distant immediate.

When you see that line on the chart showing your natural decline trajectory dropping into the “Very Poor” range at age 58, that’s no longer an abstract concern about “health”, it’s a concrete, visual representation of a future you probably don’t want. And when you see the optimisation line staying in the “Good” range through age 80, that’s a concrete representation of what’s possible if you put in consistent work.

Is it perfectly accurate? No. Will your actual results match these lines exactly? Almost certainly not. But does it give you a reasonable, evidence-based picture of where different behavior patterns tend to lead? Absolutely.

 

These Are Best Guesses, Not Rock Solid Facts

I don’t want you to think this tool is magic, and I would rather be completely transparent with you about how I built the Triage Health Trajectory Tool. The rates of decline and improvement are based on a combination of published scientific research and my own professional judgment about what’s realistic at different ages.

For some metrics, we have rock-solid data. Cardiovascular fitness decline with age? That’s been studied extensively. We know pretty well how VO₂ max changes in sedentary populations versus trained populations across different age ranges. Metabolic markers like glucose and HbA1c in the context of lifestyle interventions? Tons of research there too.

For other metrics, the data is less clear, or it’s spread across studies with different methodologies, or it doesn’t neatly separate into “natural decline” versus “maintenance” versus “optimisation” categories. In those cases, I’ve had to make judgment calls based on my understanding of human physiology, my experience working with hundreds of clients, and my interpretation of the available research.

For example, when I say that optimisation can produce a 15% improvement in testosterone levels over one year for a 30-year-old male, that’s based on studies showing the effects of resistance training, weight loss, sleep optimisation, and stress management on testosterone. But different studies show different magnitudes of effect, and they don’t all use the same definitions of “optimisation.” So I’ve made a judgment call about what seems reasonable based on the totality of the evidence and my real-world observations.

Are these numbers definitive, precise, objective facts? No. They’re best guesses. Informed, evidence-based best guesses, but best guesses nonetheless.

Could I be off by 20% on some of the rates? Absolutely. Could some metrics respond faster or slower than I’ve projected? For sure. Could the optimal trajectory for a 50-year-old be slightly different than what I’ve modeled? Yep.

 

Why This Still Matters

Now, you might be thinking: “If this is all just approximations and best guesses, why should I trust it or base decisions on it?” Fair question, and my answer is: Because the general direction and magnitude of effects are clear, even if the precise numbers are uncertain.

Let me give you an analogy. If I told you that investing €500 a month for 30 years would give you somewhere between €800,000 and €1,200,000 (depending on market returns), would you dismiss that as useless information because it’s not precise? Of course not. You’d recognise that the range of outcomes is all way better than having $0, and you’d make decisions accordingly.

Same thing here. Even if my projection that your VO₂ max will be 43 ml/kg/min at age 80 with optimisation is off by ±15%, the range of possible outcomes (37-50 ml/kg/min) is still dramatically better than the natural decline projection of 21 ml/kg/min. The uncertainty doesn’t negate the value of the information.

The fundamental truths remain solid:

  • Sedentary lifestyles lead to significant decline across virtually all health metrics.
  • Basic consistent effort (maintenance level) meaningfully slows that decline.
  • Dedicated optimisation can often reverse decline and maintain function decades longer.
  • Small differences in behaviour compound into massive differences in outcomes over time.

Those patterns are unquestionable. The exact rates might vary by individual, but the direction is clear.

 

How to Think About Uncertainty

Here’s how I want you to approach these projections: Use them as a planning tool, not a prediction. Don’t look at your results and think “My VO₂ max will be exactly 43.2 ml/kg/min at age 75.” Instead, think “If I pursue optimisation, I can likely maintain cardiovascular fitness in the ‘Good’ or ‘Optimal’ range well into my 70s, whereas natural decline would put me in the ‘Poor’ or ‘Very Poor’ range.”

Don’t fixate on the specific numbers. Focus on:

  • The relative gaps between trajectories. If optimisation is 50% better than natural decline for a metric, that pattern is likely real even if the absolute numbers are off
  • The timing of band transitions. When you cross from “Good” to “Average” might vary, but the fact that optimisation delays that transition by years or decades is reliable
  • The metrics where you have the most to gain. If several metabolic markers show huge gaps between natural decline and optimisation, that’s telling you where to focus, regardless of whether the exact values are perfectly accurate

 

The Bottom Line

This tool is built on the best available evidence, filtered through professional experience and clinical judgment. It’s not a crystal ball, and I’m not pretending it is. But it’s also not random speculation. Think of it like a weather forecast. When the meteorologist says there’s a 70% chance of rain tomorrow, they’re not claiming perfect knowledge of the future. They’re giving you their best assessment based on models, data, and experience. And you make decisions accordingly; you might bring an umbrella, even though you know the forecast could be wrong.

Same here. These projections show you the likely outcomes based on different behaviour patterns. Your actual results will vary based on genetics, adherence, life circumstances, and factors we can’t fully predict. But the patterns are real, the principles are sound, and the general direction is clear.

Use this information to inform your decisions, not to predict your future with false precision. And remember that regardless of what the specific numbers turn out to be, the trajectory you choose will profoundly shape your health span and quality of life. The uncertainty doesn’t make the information less valuable. It makes it appropriately humble. And that’s how all good science should be.

 

The Health Targets Trajectory

Alright, let’s get into the nuts and bolts of how these projections actually work. I’ve already covered what the different health targets mean and their optimal ranges in detail in our other calculator (the Triage Health Targets Calculator, if you want a deep dive into why these specific metrics matter and what the ranges mean, go read that article).

So I’m not going to rehash all of that here. What I am going to do is show you the actual trajectory rates that power this calculator, the percentages and rates of change that determine where each of those three coloured lines goes on your charts.

 

Understanding The Trajectory Rates

This section lays out the complete trajectory rates for all 28 health metrics in the calculator. These are organised by category, and for each metric, you’ll see how it changes across different age ranges under three different scenarios.

Natural = No intervention. This is the sedentary modern adult trajectory: minimal exercise, typical Western diet, inadequate sleep, high stress. Basically, the default path for someone who’s let modern life take over.

Maintenance = Moderate effort. We’re talking 2-3x/week exercise (nothing crazy, just consistent movement), a decent diet with attention to protein and vegetables, reasonable sleep, basic stress management. This is “I care about my health but I am not obsessed about it” or the “minimum effective dose”.

Optimisation = Elite effort. Training 4-6x/week with a structured program, nutrition dialed in and tracked, sleep prioritised, and stress managed proactively. This is treating your health like a serious athletic pursuit.

Initial boost = Many metrics show a one-time improvement period when you first start optimisation. This is that “newbie gains” phase where your body responds dramatically to the new stimulus. The duration shows how long this initial improvement phase lasts (usually 1-3 years), after which the metric either maintains or begins a much slower decline.

The rates are shown as percentage changes per year for most metrics (meaning they compound annually based on your current value) or absolute unit changes per year for a few metrics like FFMI and chin-ups.

 

BLOOD LIPIDS 

These are your cardiovascular risk markers. The ones that determine whether you’re headed for a heart attack or stroke down the line. Let’s break down each one:

 

ApoB (g/L) – % per year

Age Range Natural Maintenance Optimisation
20-35 +0.8% 0% -20% initial (1yr) → 0%
35-50 +1.2% +0.6% 0%
50-65 +1.5% +0.8% +0.25%
65-80 +0.8% +0.4% 0%
80-100 +0.4% +0.2% 0%

50-year projection (age 30→80):

  • Natural: 0.8 g/L → 1.35 g/L (poor range)
  • Maintenance: 0.8 g/L → 1.05 g/L (average range)
  • Optimisation: 0.8 g/L → 0.68 g/L → 0.72 g/L (optimal range)

What this tells you: ApoB is arguably the single best predictor of cardiovascular disease risk. Notice how the natural trajectory shows steady increases across all age ranges, with the biggest jumps happening in midlife (35-65). This reflects the reality that sedentary adults with typical modern diets see their cholesterol markers worsen progressively with age.

The maintenance scenario halves the rate of increase, just showing up 2-3x/week and eating reasonably well makes a massive difference. But in the optimisation scenario, you actually get an initial reduction of 20% in the first year (thanks to aggressive dietary changes, weight loss if needed, consistent training and maybe even pharmaceuticals), and then you hold steady for decades. That’s the difference between ending up with concerning cardiovascular risk versus maintaining excellent heart health.

This is a super important metric to focus on, because you can think of arterial damage like compound interest on a loan, except the loan is against your future health. Every year you spend with elevated ApoB is another year of LDL particles infiltrating your arterial walls, oxidising, triggering inflammation, and slowly building atherosclerotic plaques. This is the critical difference between cardiovascular disease and something like metabolic disease: cardiovascular damage is cumulative.

You can reverse fatty liver with weight loss. You can often reverse pre-diabetes with lifestyle changes. But you can’t reverse 20 years of plaque buildup in your arteries. You can stop it from getting worse, you can stabilise existing plaques, but the damage you’ve accumulated is largely permanent.

This is why starting early matters so profoundly for cardiovascular health. If you optimise in your 20s or 30s and maintain low ApoB for life, you might reach age 70 with relatively clean arteries. If you follow the natural trajectory until age 50, then try to optimise, you’ve already got 20-30 years of plaque accumulation that you’re now stuck with.

Every year at optimal ApoB levels is a year you’re NOT accumulating damage. Every year in the poor range is a year you ARE accumulating damage. The maths is brutal but clear: minimise the total number of years spent above optimal levels. Start now, stay consistent, and avoid decades of irreversible arterial damage.

 

LDL-C (mmol/L) – % per year

Age Range Natural Maintenance Optimisation
20-35 +0.5% 0% -25% initial (1yr) → 0%
35-50 +0.8% +0.4% 0%
50-65 +1.2% +0.6% +0.2%
65-80 +0.5% +0.25% 0%
80-100 +0.25% +0.12% 0%

50-year projection (age 30→80):

  • Natural: 3.0 mmol/L → 4.5 mmol/L (poor range)
  • Maintenance: 3.0 mmol/L → 3.65 mmol/L (average range)
  • Optimisation: 3.0 mmol/L → 2.25 mmol/L → 2.35 mmol/L (good range)

What this tells you: LDL cholesterol follows a similar pattern to ApoB, as it creeps up steadily in sedentary adults, with the steepest increases in the 35-65 age range. That 50-year natural trajectory takes you from a reasonable 3.0 mmol/L to 4.5 mmol/L, which is solidly in the “increased cardiovascular risk” territory.

Optimisation can drop your LDL by 25% in the first year through dietary changes (particularly reducing saturated fat and increasing fibre) combined with weight loss and exercise. Then you maintain that improved level. We’re talking about potentially preventing decades of cardiovascular damage just by getting serious about your health in your 20s, 30s, or 40s.

 

Triglycerides (mmol/L) – % per year

Age Range Natural Maintenance Optimisation
20-35 +1.0% 0% -30% initial (1yr) → 0%
35-50 +1.5% +0.7% 0%
50-65 +1.8% +0.9% +0.3%
65-80 +1.0% +0.5% 0%
80-100 +0.5% +0.25% 0%

50-year projection (age 30→80):

  • Natural: 1.0 mmol/L → 2.05 mmol/L (average/poor border)
  • Maintenance: 1.0 mmol/L → 1.35 mmol/L (average range)
  • Optimisation: 1.0 mmol/L → 0.70 mmol/L → 0.75 mmol/L (optimal range)

What this tells you: Triglycerides are incredibly responsive to lifestyle, which is why you see such dramatic differences between trajectories. The natural path shows your triglycerides more than doubling over 50 years, as that’s the effect of increasing insulin resistance, weight gain, and poor dietary choices (particularly excess refined carbs and alcohol) compounding over time.

But the good news is that triglycerides respond fast to intervention. Cut the refined carbs, lose some weight, start training consistently, and you can see a ~30% drop in the first year. That’s why optimisation shows such a dramatic initial improvement. Triglycerides are one of those metrics where you can literally see results in your next blood test after making changes.

 

HDL Cholesterol (mmol/L) – % per year (sex-specific bands)

Age Range Natural Maintenance Optimisation
20-35 0% 0% +10% initial (1yr) → 0%
35-50 -0.2% 0% 0%
50-65 -0.3% -0.15% 0%
65-80 -0.2% -0.1% 0%
80-100 -0.1% 0% 0%

50-year projection (age 30→80):

  • Natural: 1.3 mmol/L → 1.20 mmol/L (slight decline)
  • Maintenance: 1.3 mmol/L → 1.27 mmol/L (maintained)
  • Optimization: 1.3 mmol/L → 1.43 mmol/L → 1.43 mmol/L (improved + maintained)

What this tells you: HDL is your “good” cholesterol, and unlike the others, higher is generally better (within reason). Notice how even the natural decline is relatively modest; HDL doesn’t crash with age like some other metrics. But it does tend to decline slightly, particularly in midlife.

Maintenance keeps it stable and optimisation actually improves it. That 10% initial boost from optimisation (achieved through consistent cardio and resistance training, weight loss, and perhaps a few other targets interventions) might not sound like much, but it’s clinically significant. And then you hold onto that improvement for life.

 

Blood Lipids Summary: Notice the pattern across all four lipid markers? Natural decline shows steady worsening. Maintenance roughly halves the rate of decline. Optimisation often reverses the decline initially and then maintains at much better levels. This is the compound effect in action; small annual changes adding up to dramatically different outcomes over decades.

 

BLOOD PRESSURE MARKERS

 

Blood Pressure – Systolic (mmHg) – % per year

Age Range Natural Maintenance Optimisation
20-35 +0.3% 0% -8% initial (1yr) → +0.05%
35-50 +0.5% 0% +0.1%
50-65 +0.7% +0.35% +0.15%
65-80 +0.6% +0.3% +0.2%
80-100 +0.4% +0.2% +0.2%

50-year projection (age 30→80):

  • Natural: 115 mmHg → 138 mmHg (stage 1 hypertension)
  • Maintenance: 115 mmHg → 126 mmHg (elevated)
  • Optimisation: 115 mmHg → 106 mmHg → 118 mmHg (optimal/good)

 

What this tells you: Blood pressure is interesting because it’s influenced by so many factors; arterial stiffness, body weight, sodium sensitivity, stress levels, cardiovascular fitness, and genetics. The natural trajectory shows you starting with excellent blood pressure (115 mmHg) and ending up with stage 1 hypertension (138 mmHg) by age 80.

This generally happens due to arterial stiffening with age (exacerbated by inactivity and poor diet), weight gain (especially visceral fat), declining cardiovascular fitness, chronic inflammation, poor sleep, and chronic stress. These all push blood pressure upward over time.

Something interesting about the optimisation trajectory: even with elite-level effort, blood pressure still tends to increase slightly after the initial improvement phase, particularly after age 50. That’s because some arterial stiffening with age is unavoidable, as it’s actual biological ageing, not just lifestyle-driven decline. But the rate of increase is dramatically slower, and you start from a lower baseline (that 8% initial reduction in the first year), so you stay in the optimal/good range instead of crossing into hypertension.

The maintenance trajectory keeps you in the “elevated” range, which is not great, but not terrible. Just exercising regularly and keeping your weight reasonable prevents hypertension, but doesn’t fully optimise your cardiovascular health.

 

Blood Pressure – Diastolic (mmHg) – % per year

Age Range Natural Maintenance Optimisation
20-35 +0.15% 0% -10% initial (1yr) → +0.05%
35-50 +0.25% 0% +0.08%
50-65 +0.35% +0.18% +0.12%
65-80 +0.3% +0.15% +0.12%
80-100 +0.2% +0.1% +0.1%

50-year projection (age 30→80):

  • Natural: 75 mmHg → 87 mmHg (approaching stage 1 hypertension)
  • Maintenance: 75 mmHg → 81 mmHg (good)
  • Optimisation: 75 mmHg → 68 mmHg → 77 mmHg (optimal)

What this tells you: Diastolic pressure (the bottom number) follows a similar pattern to systolic, but typically increases at a slower rate. The natural trajectory takes you from 75 mmHg (optimal) to 87 mmHg (approaching the stage 1 hypertension cutoff of 90 mmHg).

The optimisation trajectory is particularly interesting here, as you actually see a 10% reduction initially (dropping to 68 mmHg), then a very gradual increase over decades. Even at age 80, you’re still in the optimal range at 77 mmHg. That’s the power of maintaining excellent cardiovascular fitness, healthy body composition, and good lifestyle habits.

 

METABOLIC MARKERS

This is where things get real, folks. Metabolic markers are essentially your “diabetes risk dashboard”, and they tell you how well your body is handling glucose and whether you’re on the path to metabolic disease. And let me tell you, the natural trajectory for these markers in modern society is pretty brutal.

 

Fasting Glucose (mmol/L) – % per year

Age Range Natural Maintenance Optimisation
20-35 +0.3% 0% -12% initial (1yr) → 0%
35-50 +0.6% +0.1% 0%
50-65 +0.9% +0.3% 0%
65-80 +0.7% +0.3% 0%
80-100 +0.4% +0.2% 0%

50-year projection (age 30→80):

  • Natural: 5.0 mmol/L → 6.65 mmol/L (pre-diabetic!)
  • Maintenance: 5.0 mmol/L → 5.65 mmol/L (average)
  • Optimisation: 5.0 mmol/L → 4.4 mmol/L → 4.4 mmol/L (optimal)

What this tells you: This one should scare you. Look at that natural trajectory; you start at a perfectly healthy 5.0 mmol/L at age 30, and by age 80, you’re at 6.65 mmol/L, which is pre-diabetic. The cutoff for pre-diabetes is 6.1 mmol/L, and for diabetes it’s 7.0 mmol/L. You’re literally one step away from a diabetes diagnosis.

This isn’t some rare outcome, this is the typical trajectory for sedentary modern adults. We live in an obesogenic environment with ultra-processed foods everywhere, constant snacking, sedentary jobs, poor sleep, and chronic stress. All of these drive insulin resistance, which shows up as rising fasting glucose.

Notice how the rate of increase accelerates in the 50-65 age range. That’s when decades of poor metabolic health start catching up with you, combined with age-related loss of muscle mass (which is your primary glucose disposal organ).

But here’s the good news: this is one of the most responsive metrics to lifestyle intervention. Maintenance effort (just exercising 2-3x/week and eating reasonably well) keeps you in the average range. And with optimisation you actually improve your fasting glucose by 12% in the first year through weight loss, consistent training, and dietary changes, then lock in that optimal level indefinitely.

The bottom line: Metabolic disease is not an inevitable part of ageing. It’s a consequence of lifestyle choices compounded over decades. This trajectory shows that crystal clear.

 

HbA1c (mmol/mol) – % per year

Age Range Natural Maintenance Optimisation
20-35 +0.4% 0% -15% initial (1yr) → 0%
35-50 +0.7% +0.1% 0%
50-65 +1.0% +0.3% 0%
65-80 +0.8% +0.3% 0%
80-100 +0.4% +0.2% 0%

50-year projection (age 30→80):

  • Natural: 35 mmol/mol → 48.5 mmol/mol (diabetic threshold!)
  • Maintenance: 35 mmol/mol → 40.0 mmol/mol (average)
  • Optimisation: 35 mmol/mol → 29.8 mmol/mol → 29.8 mmol/mol (optimal)

What this tells you: HbA1c (glycated haemoglobin) is even more damning than fasting glucose because it reflects your average blood sugar over the past 3 months. You can’t game this test by fasting the day before; it tells the real story of your metabolic health.

Look at that natural trajectory again: starting at a healthy 35 mmol/mol at age 30, climbing to 48.5 mmol/mol by age 80. The diabetic threshold is 48 mmol/mol. You’re literally crossing into diabetes by following the standard American lifestyle for 50 years.

Now, of course, genetics play a role in your susceptibility, but the trajectory data should hopefully make it clear that a big driver is lifestyle. If “natural” (sedentary) behaviour leads you to diabetic levels, and optimisation keeps you in the optimal range, genetics are only part of the story.

The steepest increases happen in midlife (35-65), which is when people are typically most stressed, least active, sleeping poorly, and letting their nutrition slide because they’re “too busy with career and kids.” That’s also when the consequences of those choices start compounding aggressively.

Optimisation shows a 15% reduction in the first year. This is mostly driven by weight loss (especially visceral fat), resistance training (building muscle improves insulin sensitivity dramatically), cutting refined carbs, and improving sleep quality. Then you maintain that excellent level for life. We’re talking about the difference between being on multiple diabetes medications versus having the metabolic health of a fit 25-year-old at age 75.

Metabolic Markers Summary: The pattern is undeniable; modern lifestyle drives you toward metabolic disease (pre-diabetes/diabetes) and hypertension. These aren’t “diseases of ageing”, they’re diseases of lifestyle choices compounded over time. The natural trajectories cross into disease thresholds. The optimisation trajectories keep you in optimal ranges for life. The choice is yours, but now you can see exactly what that choice compounds into over 50 years.

Now, it’s worth understanding that for 99% of human evolutionary history, type 2 diabetes essentially didn’t exist. Our ancestors lived in conditions of intermittent scarcity; sometimes abundant food, often limited food, and constant movement to acquire it. The human body evolved exquisite mechanisms to store energy when available (insulin, fat storage) and mobilise it when needed (glucagon, lipolysis).

Then, in the last 50-100 years, we created an environment of chronic caloric abundance, ultra-processed foods engineered for overconsumption, and sedentary work. Your body is running Paleolithic software in a modern environment, and the result is metabolic chaos.

Your insulin system thinks you need to store every available calorie because famine might be coming. It doesn’t know that you have a refrigerator full of food and a grocery shop on every corner. Your dopamine system rewards you for high-calorie, high-palatability foods because that was adaptive when calories were scarce. It doesn’t know that those rewards are now driving obesity and metabolic disease.

This is what evolutionary biologists call a “mismatch”, where your evolved biology is mismatched to your environment. The natural trajectory in these metabolic markers isn’t really “natural” in an evolutionary sense. It’s what happens when ancient biology meets modern abundance.

The optimisation trajectory is deliberately overriding those evolved drives. You’re choosing adaptive stress (training, intermittent fasting, whole foods that don’t trigger overconsumption) over maladaptive stress (chronic sitting, constant snacking, hyperpalatable processed foods). You’re creating an environment that matches your biology, even though you live in the 21st century.

 

INFLAMMATION & IMMUNE 

Now let’s talk about inflammation, which is an underlying driver of almost every chronic disease you can name. Heart disease, diabetes, cancer, Alzheimer’s, and autoimmune conditions, all have chronic inflammation as a common thread. This is not to say inflammation is the only cause, not at all. But it is in the mix of causality.

 

hs-CRP (mg/L) – % per year

Age Range Natural Maintenance Optimisation
20-35 +1.5% 0% -40% initial (1yr) → 0%
35-50 +2.0% +0.7% 0%
50-65 +2.4% +1.2% +0.4%
65-80 +2.0% +1.0% +0.4%
80-100 +1.6% +0.8% +0.4%

50-year projection (age 30→80):

  • Natural: 1.0 mg/L → 3.5 mg/L (average/poor range)
  • Maintenance: 1.0 mg/L → 1.85 mg/L (good/average border)
  • Optimisation: 1.0 mg/L → 0.6 mg/L → 0.75 mg/L (optimal)

What this tells you: hs-CRP (high-sensitivity C-reactive protein) is your body’s general inflammation marker. It goes up when you have chronic low-grade inflammation, which is increasingly recognised as one of the key drivers of ageing and disease.

Look at those natural trajectory rates; we’re talking about 1.5-2.4% annual increases in your 30s through 60s. That’s because the typical modern lifestyle is profoundly inflammatory: processed foods, sedentary behaviour, obesity (especially visceral fat, which is metabolically active and inflammatory), poor sleep, chronic stress, and environmental toxins. All of this drives systemic inflammation higher and higher over time.

By age 80 on the natural trajectory, your CRP has more than tripled from 1.0 mg/L to 3.5 mg/L. For context, CRP levels above 3.0 mg/L are associated with high cardiovascular disease risk. You’ve literally inflamed your way into the high-risk category.

But what’s amazing about CRP is that it responds incredibly well to lifestyle intervention. That 40% initial reduction with optimisation isn’t a typo; that’s what happens when you lose excess body fat (especially visceral fat), start training consistently, clean up your diet (more whole foods, less processed junk), improve your sleep, and manage stress. Inflammation drops like a lead balloon.

Then you maintain that low level indefinitely. We’re talking about the difference between living in a state of chronic inflammation (driving disease risk) versus maintaining excellent anti-inflammatory status (protective against disease).

Even maintenance-level effort makes a huge difference; keeping CRP stable or only slightly increasing versus more than tripling over 50 years. This is low-hanging fruit for disease prevention.

 

WBC Count (×10⁹/L) – % per year

Age Range Natural Maintenance Optimisation
20-35 +0.15% 0% -15% initial (1yr) → 0%
35-50 +0.25% +0.08% 0%
50-65 +0.3% +0.15% +0.05%
65-80 +0.25% +0.12% +0.05%
80-100 +0.15% +0.08% +0.05%

50-year projection (age 30→80):

  • Natural: 6.0 ×10⁹/L → 6.9 ×10⁹/L (optimal→good range)
  • Maintenance: 6.0 ×10⁹/L → 6.5 ×10⁹/L (optimal)
  • Optimisation: 6.0 ×10⁹/L → 5.1 ×10⁹/L → 5.25 ×10⁹/L (optimal)

What this tells you: White blood cell count is a bit different from the other metrics because it’s not purely a “lower is better” situation. You need a healthy immune system, so both too low and too high are problems. But chronically elevated WBC (even within the “normal” range) is associated with inflammation, insulin resistance, and cardiovascular risk.

The natural trajectory shows a modest increase over 50 years, from 6.0 to 6.9 ×10⁹/L. That’s moving from optimal toward the good range, which sounds fine, but it reflects the chronic low-grade inflammatory state that develops with sedentary ageing.

Optimisation actually reduces WBC by 15% initially (dropping to 5.1 ×10⁹/L), then keeps it in the lower end of the optimal range long-term. This isn’t suppressing your immune system, it’s reducing the chronic inflammatory stimulus that was keeping WBC elevated.

Think of it this way: your immune system is constantly responding to the inflammatory signals from visceral fat, poor diet, lack of exercise, poor sleep, and stress. When you remove those inflammatory stimuli through optimisation, your immune system calms down, and WBC normalises to a healthier baseline.

 

Inflammation & Immune Summary: Chronic inflammation is the silent killer, and if it’s not driving disease risk behind the scenes, it is at least a co-conspirator. The natural trajectory shows steady increases in inflammatory markers. Optimisation dramatically reduces inflammation and maintains excellent anti-inflammatory status for life. This is one of the most powerful levers you have for preventing chronic disease and extending healthspan.

 

LIVER HEALTH 

Your liver is one of the most underappreciated organs in your body. It’s processing everything you eat and drink, detoxifying compounds, producing proteins, regulating blood sugar, and so much more. It’s basically your body’s chemical processing plant. And in modern society, we’re absolutely hammering it with a toxic combination of excess calories, alcohol, processed foods, and sedentary behaviour. Let’s see what that does over time.

 

ALT (U/L) – % per year

Age Range Natural Maintenance Optimisation
20-35 +0.3% 0% -25% initial (1yr) → 0%
35-50 +0.5% +0.15% 0%
50-65 +0.6% +0.25% 0%
65-80 +0.4% +0.15% 0%
80-100 +0.2% +0.1% 0%

50-year projection (age 30→80):

  • Natural: 20 U/L → 30.5 U/L (optimal→average, fatty liver risk)
  • Maintenance: 20 U/L → 24.5 U/L (optimal→good)
  • Optimisation: 20 U/L → 15 U/L → 15 U/L (optimal)

What this tells you: ALT (alanine aminotransferase) is a liver enzyme that leaks into your bloodstream when liver cells are damaged or stressed. Elevated ALT is one of the first signs of non-alcoholic fatty liver disease (NAFLD), which has become an epidemic in developed countries, we’re talking about 25-30% of adults having some degree of fatty liver.

Look at that natural trajectory: starting at a healthy 20 U/L at age 30, climbing to 30.5 U/L by age 80. That takes you from optimal straight into the average range, which in this context means “you probably have some degree of fatty liver developing.” This isn’t just a benign lab abnormality; NAFLD can progress to inflammation (NASH), fibrosis, cirrhosis, and even liver cancer.

What’s driving this is the perfect storm of modern lifestyle: excess calories (particularly from refined carbs and fructose), sedentary behaviour, obesity (especially visceral fat), insulin resistance, and sometimes alcohol. Your liver starts accumulating fat, cells get stressed and damaged, and ALT rises as a marker of that damage.

But here’s the incredibly good news: fatty liver is almost completely reversible with lifestyle changes. That 25% reduction in the first year with optimisation isn’t theoretical, that’s what happens when you lose weight (even just 5-10% of body weight can dramatically improve fatty liver), start exercising regularly, cut the refined carbs and excess fructose, and improve insulin sensitivity through resistance training.

Then you maintain that excellent level indefinitely. We’re talking about completely preventing fatty liver disease just by taking your health seriously. Maintenance effort keeps you in the good range; ALT creeps up a bit, but you avoid significant liver damage.

 

AST (U/L) – % per year

Age Range Natural Maintenance Optimisation
20-35 +0.3% 0% -25% initial (1yr) → 0%
35-50 +0.5% +0.15% 0%
50-65 +0.6% +0.25% 0%
65-80 +0.4% +0.15% 0%
80-100 +0.2% +0.1% 0%

50-year projection (age 30→80):

  • Natural: 22 U/L → 33.6 U/L (optimal→average)
  • Maintenance: 22 U/L → 27.0 U/L (optimal→good)
  • Optimisation: 22 U/L → 16.5 U/L → 16.5 U/L (optimal)

What this tells you: AST (aspartate aminotransferase) is another liver enzyme, though it’s also found in other tissues like the heart and muscle. It follows almost the exact same trajectory as ALT because both are responding to the same underlying issue; liver stress and damage from metabolic dysfunction.

The natural trajectory takes you from 22 U/L (optimal) to 33.6 U/L (average), mirroring the progression of fatty liver disease. The optimisation trajectory shows the same dramatic 25% initial improvement, then maintenance at excellent levels.

One thing I want to emphasise is when both ALT and AST are elevated together, and the ALT is higher than AST (which is typical in NAFLD), that’s a strong signal that metabolic dysfunction is driving liver damage. This isn’t about drinking too much – this is about diet, body composition, and insulin resistance.

 

Liver Health Summary: The liver is remarkably resilient, and it can regenerate and heal itself if you give it the chance. But decades of metabolic assault will drive steady increases in liver enzymes, signalling progressive damage. The natural trajectory shows you sliding toward fatty liver disease by following typical modern lifestyle patterns. Optimisation not only prevents this but actually improves liver function below your baseline. Your liver will thank you for losing weight, exercising, and cleaning up your diet.

 

KIDNEY & THYROID

Now let’s look at two organs that are critical for long-term health but often overlooked until there’s a serious problem: your kidneys and thyroid.

 

eGFR (mL/min/1.73m²) – % per year

Age Range Natural Maintenance Optimisation
20-35 0% 0% 0%
35-50 -0.5% -0.25% -0.1%
50-65 -0.7% -0.35% -0.15%
65-80 -0.8% -0.4% -0.2%
80-100 -0.6% -0.3% -0.2%

50-year projection (age 30→80):

  • Natural: 100 mL/min → 72 mL/min (average range)
  • Maintenance: 100 mL/min → 87 mL/min (good range)
  • Optimisation: 100 mL/min → 94 mL/min (optimal range)

What this tells you: eGFR (estimated glomerular filtration rate) measures how well your kidneys are filtering waste from your blood. It’s one of those metrics where some decline with age is genuinely unavoidable, you’re losing nephrons (kidney filtering units) as part of normal ageing, and there’s no way to reverse that completely.

Notice that even in your 20s and early 30s, there’s no decline in any of the three scenarios – kidney function is stable. But starting around age 35, you begin losing kidney function gradually. The question is how fast?

The natural trajectory shows a 28% decline over 50 years (100 → 72 mL/min). That takes you from optimal kidney function down to the average range. While 72 mL/min isn’t kidney failure (that doesn’t happen until you drop below 15 mL/min), it’s definitely reduced function. You’re in stage 2 chronic kidney disease at that point, which increases your risk of cardiovascular disease and can progress to more serious kidney problems.

What drives faster kidney decline? Uncontrolled hypertension (high blood pressure damages the delicate blood vessels in your kidneys), diabetes (high blood sugar is toxic to kidney tissue), obesity, chronic inflammation, certain medications (especially NSAIDs used chronically), and dehydration. Notice how all of these tie back to the metabolic and cardiovascular markers we’ve already discussed?

Optimisation slows the decline dramatically, as you’re only losing 6% over 50 years (100 → 94 mL/min), staying firmly in the optimal range. This is accomplished by controlling blood pressure, maintaining excellent blood sugar control, staying at a healthy weight, exercising regularly (which improves kidney blood flow), and avoiding nephrotoxic substances. Even maintenance effort gets you to 87 mL/min (good range), which is a huge win compared to the natural trajectory.

Key insight: You can’t completely prevent age-related kidney decline, but you can slow it to a crawl. The difference between 72 mL/min (average, bordering on concerning) and 94 mL/min (optimal, like someone 20 years younger) is massive for long-term health.

 

TSH (mIU/L) – % per year

Age Range Natural Maintenance Optimisation
20-35 +0.08% 0% 0%
35-50 +0.15% +0.08% 0%
50-65 +0.2% +0.1% +0.05%
65-80 +0.25% +0.12% +0.05%
80-100 +0.15% +0.08% +0.05%

50-year projection (age 30→80):

  • Natural: 1.5 mIU/L → 1.95 mIU/L (optimal)
  • Maintenance: 1.5 mIU/L → 1.72 mIU/L (optimal)
  • Optimisation: 1.5 mIU/L → 1.58 mIU/L (optimal)

What this tells you: TSH (thyroid stimulating hormone) is a bit different from most other metrics because it has a two-sided optimal range, and you don’t want it too high or too low. TSH is what your pituitary gland produces to tell your thyroid to make more thyroid hormone. If TSH is rising, it usually means your thyroid is becoming sluggish (hypothyroidism).

The interesting thing about this trajectory is that even in the natural decline scenario, TSH stays within the optimal range over 50 years (1.5 → 1.95 mIU/L). The increases are very modest. This reflects the fact that most people don’t develop overt thyroid dysfunction just from ageing. When it happens, it’s usually due to autoimmune issues (Hashimoto’s thyroiditis) or other specific problems, not just lifestyle factors.

That said, there is a slight upward trend with ageing in sedentary populations, and maintenance/optimisation can keep TSH even more stable. The mechanisms aren’t as clear-cut as with other markers, but stress management, adequate sleep, sufficient micronutrients (especially iodine, selenium, and zinc), and avoiding excessive endurance training (which can suppress thyroid function, especially if calories aren’t appropriate) all help maintain healthy thyroid function.

Key insight: Unlike most other metrics, thyroid function is relatively stable across the lifespan if you don’t have autoimmune or other specific thyroid issues. The lifestyle interventions that optimise other markers also tend to support healthy thyroid function, but the effects are modest. This is one metric where genetics and autoimmunity play a larger role than pure lifestyle factors.

Kidney & Thyroid Summary: Kidney function decline with age is real and unavoidable, but optimisation can slow it dramatically. The difference between maintaining excellent function versus sliding into reduced function. Thyroid function is relatively stable with ageing, though optimisation keeps it even more stable. Both organs are critical for overall health, and taking care of the metabolic and cardiovascular factors we’ve already discussed also protects these organs.

 

CARDIOVASCULAR FITNESS 

Now we’re getting to the metrics that literally predict how long you’ll live. I’m not being dramatic here – VO₂ max is one of the single strongest predictors of all-cause mortality we have. Stronger than smoking status, stronger than cholesterol, stronger than blood pressure. Let’s see why.

VO₂ Max (ml/kg/min) – % per year

Age Range Natural Maintenance Optimisation
20-35 -0.5% 0% +15% initial (2yr) → -0.2%
35-50 -1.0% -0.5% -0.1%
50-65 -1.5% -0.8% -0.3%
65-80 -2.0% -1.2% -0.6%
80-100 -3.0% -2.0% -1.5%

50-year projection (age 30→80):

  • Natural: 45 ml/kg/min → 21 ml/kg/min (poor range, high mortality risk!)
  • Maintenance: 45 ml/kg/min → 32 ml/kg/min (average/poor border)
  • Optimisation: 45 ml/kg/min → 51.8 ml/kg/min → 43.5 ml/kg/min (good range!)

What this tells you: This is the big one. VO₂ max measures your body’s maximum capacity to transport and use oxygen during exercise. It’s essentially your cardiovascular fitness distilled into a single number, and the research on its relationship to longevity is staggering.

Look at that natural trajectory; you start at a decent 45 ml/kg/min at age 30, and by age 80, you’ve dropped to 21 ml/kg/min. That’s a 53% decline. You’ve literally lost more than half your cardiovascular capacity. At 21 ml/kg/min, you’re in the “poor” range with high mortality risk. Studies show that people with VO₂ max in this range have roughly 5x the mortality risk compared to people in the “good” or “excellent” ranges.

What does 21 ml/kg/min feel like in real life? Climbing a flight of stairs is challenging. Walking up a hill leaves you breathless. Playing with your grandkids? Forget about it. You’re sitting on the sidelines watching life happen because your cardiovascular system can’t support more than minimal activity.

The decline accelerates with age; notice how you’re losing 0.5% per year in your 20s-30s, but by your 60s-70s it’s up to 2%, and in your 80s it’s 3% per year. That’s because sedentary ageing compounds on itself. As you get weaker and less fit, you move less, which makes you weaker and less fit, which makes you move even less. It’s a vicious cycle.

But now look at the optimisation trajectory. You actually improve by 15% over the first two years (45 → 51.8 ml/kg/min) through consistent cardiovascular training. Then, yes, you do decline, but at a crawl, only 0.2-0.6% per year. By age 80, you’re at 43.5 ml/kg/min, which is in the “good” range. You have the cardiovascular fitness of someone 25-30 years younger than your chronological age.

That’s not just a lab number, that’s the difference between hiking mountains, playing tennis, swimming with your grandkids at age 75, versus struggling to walk around the neighbourhood. That’s 8-12 extra years of life expectancy based on the research. That’s decades more of vitality and independence.

Even maintenance effort makes a massive difference; you end at 32 ml/kg/min, which is borderline but way better than 21. Just exercising 2-3x/week consistently keeps you functional.

The thing about VO₂ max that the numbers don’t fully capture is that this isn’t just a lab value or an academic exercise. This is your capacity to participate in life. At 45 ml/kg/min, you can hike mountains, play sports, swim in the ocean, chase your kids or grandkids, travel freely, and pursue physically demanding hobbies. Your cardiovascular system isn’t a limiting factor in what you choose to do.

At 21 ml/kg/min, climbing a flight of stairs leaves you breathless. Walking any distance is exhausting. Playing actively with grandchildren is impossible; you’re watching from a chair. Travelling becomes logistically difficult because you can’t walk through airports. Your cardiovascular capacity becomes the primary constraint on your life choices.

Philosopher Martha Nussbaum wrote about “capabilities”, which are the actual freedoms and opportunities a person has to do and be what they have reason to value. VO₂ max is a capability metric. Higher VO₂ max means more capabilities, more freedom, and more agency in your life. Lower VO₂ max means fewer capabilities, more constraints, and less agency. You simply can’t achieving your best self if you don’t look after your baseline physiology.

This trajectory isn’t about adding years to your life. It’s about adding capabilities to your years. It’s about remaining the protagonist of your own story instead of becoming a side character limited by your cardiovascular system.

 

Resting Heart Rate (bpm) – % per year

Age Range Natural Maintenance Optimisation
20-35 0% 0% -12% initial (2yr) → 0%
35-50 +0.08% 0% 0%
50-65 +0.12% +0.04% 0%
65-80 +0.15% +0.08% 0%
80-100 +0.1% +0.08% 0%

50-year projection (age 30→80):

  • Natural: 65 bpm → 69 bpm (good range)
  • Maintenance: 65 bpm → 66 bpm (good range)
  • Optimisation: 65 bpm → 57 bpm → 57 bpm (optimal range!)

What this tells you: Resting heart rate (RHR) is your heart rate when you’re sitting quietly, fully rested. It’s a simple but powerful marker of cardiovascular efficiency. A lower RHR generally indicates that your heart is strong and efficient, it doesn’t have to beat as many times per minute to circulate blood through your body.

The natural trajectory shows a modest increase from 65 to 69 bpm over 50 years. That’s not catastrophic, both values are in the “good” range, but it reflects declining cardiovascular fitness. Your heart has to work a little harder to do the same job as you age sedentarily.

Optimisation produces a dramatic 12% reduction over the first two years (65 → 57 bpm) through consistent cardiovascular training. Your heart literally becomes a stronger, more efficient pump. Then you maintain that improved RHR for life. We’re talking about 8-12 fewer beats per minute, which over the course of a day is about 11,500-17,000 fewer heartbeats. Your heart is literally working less hard to keep you alive.

Athletes often have RHRs in the 40s or low 50s. Elite endurance athletes can be in the 30s. A RHR of 57 is excellent for a general population adult, and maintaining that into your 70s and 80s is a clear marker of superior cardiovascular health.

 

HRV – rMSSD (ms) – % per year

Age Range Natural Maintenance Optimisation
20-35 -0.3% 0% +25% initial (2yr) → -0.15%
35-50 -0.5% -0.2% -0.2%
50-65 -0.7% -0.3% -0.25%
65-80 -0.7% -0.35% -0.3%
80-100 -0.6% -0.3% -0.3%

50-year projection (age 30→80):

  • Natural: 60 ms → 41 ms (average range)
  • Maintenance: 60 ms → 52 ms (good range)
  • Optimisation: 60 ms → 75 ms → 61 ms (good/optimal range)

What this tells you: HRV (heart rate variability) measures the variation in time between consecutive heartbeats. Counter-intuitively, higher variability is better, as it generally indicates that your autonomic nervous system is healthy and responsive. Low HRV is associated with chronic stress, poor recovery, inflammation, and increased mortality risk.

HRV naturally declines with age because your autonomic nervous system becomes less flexible. The natural trajectory shows a ~32% decline over 50 years (60 → 41 ms), taking you from the good range down to average.

But optimisation can actually improve HRV by ~25% over the first two years through a combination of cardiovascular training, stress management, sleep optimisation, and recovery practices. Then, yes, you do decline, but much more slowly. By age 80, you’re still in the good/optimal range at 61 ms.

HRV is particularly sensitive to lifestyle factors beyond just exercise, and sleep quality, stress levels, alcohol consumption, and recovery practices all have major impacts. This is one metric where the “optimisation” part includes things like meditation, proper sleep hygiene, and stress management, and not just physical training.

Cardiovascular Fitness Summary: These three metrics together paint a picture of your cardiovascular system’s capacity and efficiency. The natural trajectory shows significant decline, especially in VO₂ max. Optimisation not only prevents most of that decline but actually improves all three metrics initially. This is the difference between being a vibrant, active 80-year-old versus being frail and limited. The research is crystal clear: cardiovascular fitness is your longevity insurance policy.

 

STRENGTH

Now let’s talk about strength, which is your insurance policy against frailty, and your ticket to functionality in daily life. Strength decline with age is absolutely brutal in sedentary populations, but it’s also highly preventable. Let’s look at the numbers.

 

Squat 1RM (×BW ratio) – % per year

Age Range Natural Maintenance Optimisation
20-35 -0.3% 0% +25% initial (2yr) → -0.1%
35-50 -0.8% -0.3% -0.15%
50-65 -1.2% -0.6% -0.3%
65-80 -1.5% -0.8% -0.5%
80-100 -2.0% -1.2% -0.8%

50-year projection (age 30→80):

  • Natural: 1.5×BW → 0.75×BW (poor range, 50% loss!)
  • Maintenance: 1.5×BW → 1.15×BW (average range)
  • Optimisation: 1.5×BW → 1.88×BW → 1.50×BW (maintained!)

What this tells you: The squat is often considered to be the king of lower body strength exercises, and lower body strength is absolutely critical for maintaining independence as you age. Your ability to get up from a chair, climb stairs, and walk long distances, all depends on leg strength. I don’t necessarily think that you have to barbell back squat, but you do need strong legs, and we have to standardise to something. But other exercises that train this same pattern as just as valid (and this hold for the other movements too, so I won’t be repeating this same statement each time).

The natural trajectory is here is pretty devastating: 50% strength loss over 50 years. You start able to squat 1.5× your bodyweight (which is decent for an average adult), and by age 80, you can barely squat 0.75× bodyweight. That’s borderline functional impairment. People who can’t squat at least their bodyweight often struggle with basic activities of daily living.

Why does this happen? A large part of it is due to sarcopenia, which is the age-related loss of muscle mass and strength. If you don’t use your muscles, you lose them, and sedentary ageing means you’re not providing any stimulus for your body to maintain muscle mass. The decline accelerates after age 50, which is when most people really start to feel the effects.

But look at optimisation, you actually improve by 25% over the first two years (1.5×BW → 1.88×BW) through progressive resistance training. Then you decline very slowly, and by age 80, you’re back where you started at 1.5×BW. You’ve completely prevented the 50% loss. You’re as strong at 80 as you were at 30. 

That’s the difference between needing a walker and hiking trails. That’s the difference between needing help getting off the toilet and being fully independent. That’s the difference between moving into assisted living at 75 and living independently until you’re 90+.

Now, I am assuming a decline with the optimisation model, after the initial increase, purely because most people aren’t able to train effectively beyond the beginner/intermediate stage (~2 years), and don’t want to get something like coaching. However, you could actually have this improving for years into the future, and even starting at something liek 20, you may not see your true peak until your late 30s or early 40s. This is also true for the rest of the strength metrics.

 

Deadlift 1RM (×BW ratio) – % per year

Age Range Natural Maintenance Optimisation
20-35 -0.3% 0% +30% initial (2yr) → -0.1%
35-50 -0.8% -0.3% -0.15%
50-65 -1.2% -0.6% -0.3%
65-80 -1.5% -0.8% -0.5%
80-100 -2.0% -1.2% -0.8%

50-year projection (age 30→80):

  • Natural: 2.0×BW → 1.0×BW (poor range, 50% loss!)
  • Maintenance: 2.0×BW → 1.53×BW (average range)
  • Optimisation: 2.0×BW → 2.6×BW → 2.08×BW (improved!)

What this tells you: The deadlift is often considered to be the ultimate test of total body strength as it utilises the posterior chain, grip, core stability, and pretty much everything else to some extent. It’s also incredibly functional, as it’s literally the movement pattern of picking something up off the ground, which you do constantly in daily life.

Same story as the squat: 50% natural loss over 50 years. But with optimisation you improve by 30% initially (2.0×BW → 2.6×BW), then end up stronger at age 80 (2.08×BW) than you were at age 30 (2.0×BW). You’ve not just prevented decline, you’ve actually improved over your lifespan. You might think this is unrealistic, but there are many, many videos online showing men and women in their 80s retaining a high degree of strength well into their 80s, and even 90s.

This is possible because most people at age 30 aren’t anywhere near their genetic potential for strength. They’ve never trained seriously. So when you start training properly in your 30s, 40s, or even 50s, you can make significant gains that offset age-related decline for decades.

 

Bench Press 1RM (×BW ratio) – % per year

Age Range Natural Maintenance Optimisation
20-35 -0.4% 0% +20% initial (2yr) → -0.15%
35-50 -1.0% -0.4% -0.2%
50-65 -1.4% -0.7% -0.35%
65-80 -1.8% -1.0% -0.6%
80-100 -2.2% -1.4% -1.0%

50-year projection (age 30→80):

  • Natural: 1.2×BW → 0.52×BW (poor range, 57% loss!)
  • Maintenance: 1.2×BW → 0.80×BW (average/poor border)
  • Optimisation: 1.2×BW → 1.44×BW → 1.02×BW (average range)

What this tells you: Upper body strength declines even faster than lower body, so you will notice those steeper percentage losses per year, especially after age 50. The natural trajectory shows a 57% loss, which is even worse than squats and deadlifts.

Upper body declines faster because you use your legs for basic locomotion even if you’re sedentary, but upper body strength? Most sedentary people barely use their upper body for anything challenging. No pushing, pulling, or carrying heavy loads means rapid muscle atrophy.

At 0.52×BW bench press (the natural trajectory endpoint), you’re struggling to push yourself up from the floor, having difficulty opening jars, and struggling to lift luggage into overhead compartments. That’s functional impairment territory.

Optimisation improves you by 20% initially (1.2×BW → 1.44×BW), then you end at 1.02×BW at age 80. That’s still a decline from your peak, but it’s the difference between being strong and functional versus being weak and struggling with basic tasks.

 

Chin-ups (reps) – absolute reps per year

Age Range Natural Maintenance Optimisation
20-35 -0.15 reps 0 reps +40% initial (2yr) → -0.05 reps
35-50 -0.3 reps -0.1 reps -0.05 reps
50-65 -0.5 reps -0.2 reps -0.1 reps
65-80 -0.7 reps -0.35 reps -0.2 reps
80-100 -1.0 reps -0.6 reps -0.4 reps

50-year projection (age 30→80):

  • Natural: 10 reps → 2 reps (poor range, 80% loss!)
  • Maintenance: 10 reps → 6 reps (average range)
  • Optimisation: 10 reps → 14 reps → 10 reps (maintained!)

What this tells you: Chin-ups are one of the hardest bodyweight exercises because they require high relative strength, as you have to pull your entire bodyweight up against gravity. They’re also incredibly functional, testing grip strength, pulling strength, and core stability all at once.

The natural trajectory is absolutely brutal: 80% loss over 50 years. You go from being able to do 10 chin-ups at age 30 to barely managing 2 at age 80. Most people in that situation literally can’t do a single chin-up; 2 reps is an average that includes some people who still do a few.

At 2 reps, you have almost no upper body pulling strength left. You’d struggle to pull yourself up if you fell, have difficulty climbing anything, and can’t hang from a bar for more than a few seconds. This is frailty territory.

Optimisation lets you improve by 40% over the first two years (10 → 14 reps), then you end right back where you started at 10 reps at age 80. You’ve prevented the 80% loss completely. You’re as strong relative to your bodyweight at 80 as you were at 30.

Strength Summary: The pattern across all four strength metrics is consistent and devastating in the natural trajectory: 50-80% losses by age 80, leading to functional impairment and frailty. But optimisation not only prevents this decline, it often allows you to improve initially and then maintain or even exceed your starting strength. Maintenance effort halves the rate of decline, keeping you functional but not optimal. It should hopefully be pretty clear that resistance training is non-negotiable for healthy ageing.

 

Sarcopenia: The Silent Thief of Independence

The ancient Greeks had a concept called ataraxia, which means freedom from disturbance, and tranquillity achieved through self-sufficiency. The Stoics expanded this and believed that true freedom comes from being dependent on no one, needing nothing you cannot provide for yourself. Sarcopenia (the age-related loss of muscle mass and strength shown in these trajectories) is the destruction of that self-sufficiency. It’s not just about being weak. It’s about losing the capacity for independence.

When you can’t squat your bodyweight, you struggle to get off the toilet unassisted. When you lose 80% of your pulling strength, you can’t pull yourself up if you fall. When you can’t carry shopping bags or lift luggage, you need help with basic tasks. This is how independence dies. It rafrely happens suddenly, but rather it happens through the slow erosion of physical capacity.

The natural trajectory shows 50-85% strength losses by age 80. That’s not inevitable biological ageing, that’s the result of decades of disuse. Your muscles operate on a “use it or lose it” principle, and if you don’t provide a stimulus for your body to maintain muscle, it won’t. Muscle is metabolically expensive; your body won’t maintain tissue it doesn’t need.

But the optimisation trajectory shows you can maintain, or in some cases exceed, your age-30 strength levels at age 80. Most people at age 30 are nowhere near their genetic potential for strength. They’ve never trained seriously. So when you start training properly at 30, 40, or even 50, you can build enough strength that even decades of slow decline leave you stronger than where you started.

This is perhaps the most actionable intervention in this entire calculator. You cannot significantly increase your genetic cardiovascular capacity beyond what training can achieve. But you can dramatically increase your strength at any age. 

Strength training isn’t vanity. It’s not about looking good in a mirror. It’s about maintaining the physical capacity for independent living. It’s about self-sufficiency; needing no one, and capable of everything your life requires.

 

The overall message from cardiovascular fitness and strength metrics is hopefully unambiguous: your physical capacity doesn’t have to decline dramatically with age. The “inevitable” decline we see in the general population is largely a consequence of inactivity, not true biological ageing. Train consistently throughout your life, and you can maintain excellent function well into your 80s and beyond.

 

BODY COMPOSITION 

Body composition is where everything comes together, as it’s the physical manifestation of all your lifestyle choices around diet, exercise, sleep, and stress management. The natural trajectory for body composition in modern society is unfortunately absolutely disastrous. Let’s break it down.

 

Body Fat % – % per year

Age Range Natural Maintenance Optimisation
20-35 +0.25% 0% -12% initial (2yr) → +0.08%
35-50 +0.4% +0.15% +0.12%
50-65 +0.5% +0.2% +0.15%
65-80 +0.3% +0.15% +0.12%
80-100 +0.15% +0.08% +0.08%

50-year projection (age 30→80):

  • Natural: 15% → 25.8% (poor range, obese!)
  • Maintenance: 15% → 19.5% (good/average border)
  • Optimisation: 15% → 13.2% → 18.2% (good range)

What this tells you: This is one of the most visually obvious trajectories because you can literally see it happening in the mirror and on the scale. The natural trajectory shows a 72% increase in body fat percentage over 50 years; you go from a lean 15% body fat at age 30 to 25.8% at age 80, which crosses into the obese category for most people. 

Let’s be clear about what this means: if you weigh 75 kg at 15% body fat, you have 11.25 kg of fat. At 25.8% body fat (assuming you stay at 75 kg, which most people don’t), you’d have 19.35 kg of fat. But most people don’t stay the same weight. They gain weight and increase body fat percentage, which means they’re gaining fat while losing muscle simultaneously. It’s the worst possible combination.

This happens due to the obesogenic environment we live in: ultra-processed foods everywhere, massive portion sizes, constant food availability, sedentary jobs, poor sleep, and chronic stress. All of these drive a slow, steady accumulation of body fat. The rate accelerates in midlife (35-65) when metabolism slows, activity typically decreases, and muscle mass starts declining if you’re not training.

Optimisation shows a 12% reduction over the first two years (15% → 13.2%) through fat loss which can be relatively easily accomplished through a caloric appropriate diet, sufficient protein intake, resistance training to preserve muscle, and cardio for additional calorie burn. Then, yes, you do gradually gain some fat back over decades, but you end at 18.2%, which is still in the good range. You’ve prevented obesity and maintained a relatively lean body composition for life. Of course, if you learn the skills to manage your body fat effectively, you can actually keep it where you want it. However, life has a way of getting in the way of the best laid plans of mice and men.

Even maintenance keeps you borderline at 19.5%, which is not optimal, but you’ve avoided crossing into obesity. Just exercising regularly and not overeating dramatically slows fat gain.

Key insight: Body fat gain is not inevitable with ageing. It’s a consequence of energy imbalance (eating more than you burn) compounded over decades. The “middle-age spread” is a choice, not destiny (keep in mind that just because something is a choice, doesn’t mean it is easy; some choices are incredibly hard).

 

Waist Circumference (cm) – % per year

Age Range Natural Maintenance Optimisation
20-35 +0.25% 0% -12% initial (1yr) → +0.08%
35-50 +0.4% +0.15% +0.12%
50-65 +0.5% +0.2% +0.15%
65-80 +0.3% +0.15% +0.12%
80-100 +0.15% +0.08% +0.08%

50-year projection (age 30→80):

  • Natural: 85 cm → 104.5 cm (poor range)
  • Maintenance: 85 cm → 95.8 cm (good/average)
  • Optimisation: 85 cm → 74.8 cm → 82.0 cm (optimal/good)

What this tells you: Waist circumference is actually a better predictor of metabolic disease risk than BMI or even potentially body fat percentage, because it specifically tracks visceral fat, which is the metabolically active fat around your organs that drives insulin resistance, inflammation, and cardiovascular disease.

The natural trajectory is brutal here, as your waist expands by nearly 20 cm (almost 8 inches) over 50 years. You go from 85 cm (33.5 inches) (a lean, healthy waist) to 104.5 cm (41 inches), which is solidly in the high-risk category for metabolic disease. For men, a waist circumference above 102 cm is high risk; for women, it’s above 88 cm.

This isn’t just about aesthetics or fitting into your jeans; this is about disease risk. That extra visceral fat is pumping out inflammatory cytokines, driving insulin resistance, raising your blood pressure, and worsening your lipid profile. It’s metabolically toxic.

Optimisation shows a dramatic 12% reduction in the first year (85 cm → 74.8 cm) through fat loss, particularly targeting visceral fat through diet and exercise. Then you gradually gain some back, ending at 82.0 cm, which is still in the optimal/good range. You’ve prevented the metabolic consequences of abdominal obesity.

 

BMI (kg/m²) – % per year

Age Range Natural Maintenance Optimisation
20-35 +0.25% +0.05% -8% initial (1yr) → +0.02%
35-50 +0.4% +0.1% +0.03%
50-65 +0.5% +0.15% +0.05%
65-80 +0.3% +0.12% +0.06%
80-100 +0.15% +0.08% +0.06%

50-year projection (age 30→80):

  • Natural: 24.7 → 30.5 (obese!)
  • Maintenance: 24.7 → 27.4 (overweight)
  • Optimisation: 24.7 → 22.7 → 23.3 (optimal)

What this tells you: BMI (Body Mass Index) gets a lot of criticism because it doesn’t distinguish between muscle and fat, and that’s valid. A muscular athlete can have a “high” BMI despite being lean, but at the population level, it’s still a useful metric because most people aren’t heavily muscled athletes.

The natural trajectory takes you from 24.7 (upper end of normal weight) to 30.5 (obese) (the cutoff is 30.0). That’s a massive shift. If you’re 175 cm tall, that’s going from 76 kg to 93 kg, which is a 17 kg (37 lb) weight gain. And remember, this isn’t muscle; the FFMI data (coming next) shows you’re losing muscle over this period. This is pure fat gain.

By age 80 on the natural trajectory, you’ve crossed into obesity, with all the associated health risks: type 2 diabetes, cardiovascular disease, joint problems, cancer risk, reduced mobility, and decreased quality of life.

Optimisation reduces BMI by 8% initially (24.7 → 22.7) through fat loss while maintaining or building muscle, then keeps you in the optimal range (22.7 → 23.3) for life. Even maintenance keeps you in the overweight range (27.4), which isn’t ideal but is far better than obesity.

Key insight: The “typical” adult weight gain of 0.5-1 kg per year might seem trivial, but compound that over 30-40 years and you’ve gained 15-40 kg. That’s how people go from healthy weight to obese without noticing until the damage is done.

 

WHtR (ratio) – % per year

Age Range Natural Maintenance Optimisation
20-35 +0.3% +0.1% -8% initial (1yr) → +0.08%
35-50 +0.4% +0.15% +0.1%
50-65 +0.5% +0.2% +0.12%
65-80 +0.3% +0.15% +0.1%
80-100 +0.15% +0.08% +0.05%

50-year projection (age 30→80):

  • Natural: 0.472 → 0.581 (poor range)
  • Maintenance: 0.472 → 0.532 (good range)
  • Optimisation: 0.472 → 0.434 → 0.476 (optimal/good)

What this tells you: WHtR (Waist-to-Height Ratio) is calculated by dividing your waist circumference by your height. It’s an even better predictor of metabolic disease risk than waist circumference alone because it accounts for body size. The rule of thumb is simple: keep your waist circumference less than half your height.

The natural trajectory takes you from 0.472 (good, just under the 0.5 threshold) to 0.581 (poor, well above the threshold). At 0.581, your waist is 58% of your height. If you’re 180 cm tall, that’s a 105 cm waist, which is a massive metabolic disease risk.

Optimisation drops you to 0.434 initially (your waist is only 43% of your height), then keeps you in the optimal/good range (0.476) for life. You’re maintaining that simple rule of waist less than half your height.

Research shows WHtR above 0.5 is associated with significantly increased risk of cardiovascular disease, diabetes, and all-cause mortality. The natural trajectory puts you deep into that high-risk zone. Optimisation keeps you in the safe zone for life.

 

FFMI (Fat-Free Mass Index) – absolute units per year

Age Range Natural Maintenance Optimisation
20-35 0 units 0 units +10% initial (3yr) → 0 units
35-50 -0.25 units 0 units 0 units
50-65 -0.4 units -0.15 units 0 units
65-80 -0.6 units -0.3 units -0.15 units
80-100 -0.8 units -0.5 units -0.3 units

50-year projection (age 30→80):

  • Natural: 20 → 15.0 (poor range, severe sarcopenia!)
  • Maintenance: 20 → 18.3 (average/good border)
  • Optimisation: 20 → 22 → 20.8 (improved!)

What this tells you: FFMI (Fat-Free Mass Index) is like BMI, but only counting your lean body mass (muscle, bone, organs, everything that’s not fat). It’s calculated by dividing your fat-free mass by your height squared. It’s the best metric we have for tracking muscle mass over time.

The natural trajectory is absolutely devastating here. You lose 5 FFMI points over 50 years, dropping from 20 (decent) to 15.0 (severe sarcopenia). That’s a 25% loss of muscle mass. If you’re 175 cm tall, that’s going from about 61 kg of lean mass to 46 kg of lean mass, which 15 kg (33 lb) of muscle loss.

This is sarcopenia in action. At FFMI 15, you’re struggling with basic activities, at high risk of falls and fractures, and probably need assistance with daily living.

But look at the optimisation trajectory: you actually improve by 10% over the first three years (20 → 22) through progressive resistance training and sufficient protein intake. You’re building muscle even as you age. Then you maintain that improved level, ending at 20.8 at age 80; you’ve not just prevented the 25% loss, you’ve actually ended up with more muscle than you started with.

Even maintenance prevents most of the loss (20 → 18.3), keeping you functional and independent.

Key insight: The combination of body fat gain and muscle loss is what drives the “skinny-fat” and frail phenotypes we see in aging populations. You end up heavier but weaker, with more fat and less muscle. Optimisation reverses this completely; you end up leaner and more muscular at 80 than you were at 30.

 

Body Composition Summary: The natural trajectory across all five metrics shows the same devastating pattern: fat gain, muscle loss, expanding waistlines, crossing into overweight/obese categories, and developing severe sarcopenia. This is what happens when you let modern lifestyle run its course for 50 years.

But optimisation reverses the entire pattern. You can actually improve your body composition in your 30s, 40s, and even 50s through consistent training and nutrition, then maintain excellent composition for life. Even maintenance effort prevents most of the decline. The bottom line is that body composition decline is not an inevitable part of ageing. It’s an inevitable part of sedentary ageing. 

 

RECOVERY

Recovery is the foundation that everything else is built on. You can’t out-train poor recovery, and the single most important recovery tool you have is sleep. Let’s see what happens to sleep across the lifespan.

 

Sleep Quantity (hours) – % per year

Age Range Natural Maintenance Optimisation
20-35 -0.008% 0% +8% initial (1yr) → 0%
35-50 -0.012% -0.004% 0%
50-65 -0.015% -0.008% 0%
65-80 -0.015% -0.008% 0%
80-100 -0.012% -0.008% 0%

50-year projection (age 30→80):

  • Natural: 7.5 hrs → 7.45 hrs (minimal change)
  • Maintenance: 7.5 hrs → 7.48 hrs (minimal change)
  • Optimisation: 7.5 hrs → 8.1 hrs → 8.1 hrs (optimal)

What this tells you: Sleep is interesting because it’s one of the few metrics where the natural trajectory doesn’t show catastrophic decline. You go from 7.5 hours to 7.45 hours over 50 years, which is barely noticeable. Sleep duration is relatively stable with aging (though sleep quality often declines, which this metric doesn’t capture).

But 7.5 hours isn’t optimal for most people. The research consistently shows that 7-9 hours is the sweet spot for health, performance, and longevity. Most adults need closer to 8 hours, some need 9. Very few genuinely thrive on less than 7.

The natural and maintenance trajectories hover around 7.5 hours, which is not terrible, but not optimal. This reflects the reality that most adults chronically under-sleep due to work schedules, social obligations, screens before bed, stress, and poor sleep hygiene.

Optimisation shows an 8% improvement in the first year (7.5 → 8.1 hours) through sleep prioritisation: consistent sleep schedule, dark/cool bedroom, no screens before bed, stress management, limiting alcohol and caffeine, etc. Then you maintain that 8.1 hours for life.

Why this matters more than the numbers suggest: Sleep is the multiplier on everything else. Inadequate sleep (even just getting 7 instead of 8 hours) impairs:

  • Muscle protein synthesis (your gains from training are reduced)
  • Insulin sensitivity (your blood sugar control worsens)
  • Appetite regulation (you eat more and crave junk food)
  • Recovery (your HRV drops, resting heart rate rises)
  • Cognitive function (decision-making, willpower, focus all decline)
  • Immune function (you get sick more often)
  • Hormone production (testosterone, growth hormone production suffers)

That extra 0.6 hours (36 minutes) per night from optimisation might not sound like much, but compound that over a year: 36 minutes × 365 days = 219 hours = 9 full days of additional sleep per year. Over 50 years, that’s 450 additional days (well over a year) of sleep. That’s massive for recovery, adaptation, and health.

Key insight: Most people accept chronic under-sleeping as normal because “everyone does it.” But optimisation is about recognising that sleep is non-negotiable for health and performance, and structuring your life to prioritise it. The 8% improvement is small in percentage terms but enormous in impact on all the other metrics we’ve discussed.

 

HORMONES 

Finally, let’s talk about testosterone, the hormone that’s critical for muscle mass, strength, bone density, libido, mood, energy, and metabolic health in men. (Note: I’m focusing on men here because testosterone trajectories are much more dramatic and clinically relevant in males. Women have testosterone too, but at much lower levels and with different trajectories that aren’t easily mapped with a tool like this.)

 

Testosterone – Men (nmol/L) – % per year

Age Range Natural Maintenance Optimisation
20-35 0% 0% +15% initial (1yr) → 0%
35-50 -0.6% -0.3% -0.2%
50-65 -0.8% -0.4% -0.3%
65-80 -0.6% -0.4% -0.35%
80-100 -0.35% -0.3% -0.3%

50-year projection (age 30→80):

  • Natural: 22 nmol/L → 13.5 nmol/L (average range)
  • Maintenance: 22 nmol/L → 17.2 nmol/L (good range)
  • Optimisation: 22 nmol/L → 25.3 nmol/L → 20.8 nmol/L (optimal range!)

What this tells you: Testosterone naturally declines with age in men, and there’s no way around this. The question is whether you decline gradually and maintain healthy levels, or whether you crash into low-T territory with all its consequences.

The natural trajectory shows a ~39% decline over 50 years (22 → 13.5 nmol/L). You start at a healthy 22 nmol/L at age 30, and by age 80, you’re at 13.5 nmol/L, which is in the average range but at the lower end. Some men following this trajectory will drop below 10 nmol/L (the threshold for hypogonadism diagnosis in many labs) and experience symptoms: low energy, reduced muscle mass, increased fat gain, low libido, erectile dysfunction, depression, and poor recovery from training.

What drives faster testosterone decline? Obesity (fat tissue contains aromatase, which converts testosterone to estrogen), sedentary lifestyle, poor sleep, chronic stress (cortisol suppresses testosterone production), excess alcohol, certain medications, and environmental factors (endocrine disruptors).

But look at the optimisation trajectory: you actually improve by 15% in the first year (22 → 25.3 nmol/L) through lifestyle optimisation. Then you decline, but much more slowly (only 0.2-0.35% per year), ending at 20.8 nmol/L at age 80. You’re still in the optimal range at 80, with testosterone levels higher than many sedentary 50-year-olds. You’ve prevented the 39% crash and maintained excellent hormone production for life.

Maintenance effort gets you to 17.2 nmol/L (good range), which is not optimal but far better than 13.5. Just exercising regularly, sleeping decently, and maintaining a healthy body weight slows the decline significantly.

Why this matters: Testosterone isn’t just about libido and “manliness” (though those matter too). It’s fundamentally important for:

  • Maintaining muscle mass (testosterone is anabolic – low T accelerates sarcopenia)
  • Bone density (low T increases osteoporosis risk)
  • Metabolic health (low T is associated with insulin resistance and metabolic syndrome)
  • Cardiovascular health (the relationship is complex, but very low T increases cardiovascular risk)
  • Mood and cognition (low T is associated with depression, brain fog, and cognitive decline)
  • Recovery and adaptation (low T impairs your ability to adapt to training stress)

Men with testosterone in the optimal range (like the optimisation trajectory maintains) have better body composition, stronger muscles, denser bones, better mood, higher energy, better sexual function, and lower disease risk compared to men with average or low testosterone.

Key insight: The “normal ageing” decline in testosterone is partly inevitable (the testes produce less as you age), but it’s massively accelerated by poor lifestyle. The difference between 13.5 nmol/L (natural) and 20.8 nmol/L (optimisation) at age 80 is the difference between feeling old and struggling versus feeling vital and capable.

Some men will look at the optimisation trajectory and think “that’s still a decline from the peak of 25.3 nmol/L” and consider testosterone replacement therapy (TRT). That’s a personal decision that should be made with a knowledgeable physician. But what the trajectory shows is that lifestyle optimisation alone can maintain excellent testosterone levels for life without needing exogenous hormones for most men.

 

The Complete Picture

We’ve now walked through all the health metrics tracked in the Triage Health Trajectory Tool. Let me pull back and show you the big picture:

Every single metric shows the same fundamental pattern:

  1. Natural decline = sedentary modern lifestyle leads to progressive deterioration, often crossing into disease thresholds
  2. Maintenance = basic consistent effort (2-3x/week exercise, decent nutrition, reasonable sleep) roughly halves the rate of decline
  3. Optimisation = elite effort (4-6x/week training, strict nutrition, sleep prioritisation) often improves metrics initially, then maintains excellent levels for life

The compound effect is undeniable: Small percentage changes per year (often less than 1%) compound over 30-50 years into massive differences in outcomes. The gap between trajectories grows exponentially over time.

Starting early matters, but it’s never too late: The biggest gains from optimisation happen when you start young and maintain for decades. But even starting at 40, 50, or 60, you can make dramatic improvements and slow/prevent further decline.

These aren’t isolated metrics: Your body is an integrated system. Improving cardiovascular fitness helps metabolic markers. Losing fat reduces inflammation. Building muscle improves insulin sensitivity. Sleeping well supports testosterone. It’s all connected.

The choice is yours: You now have the data. You can see exactly where each trajectory leads. The natural path leads to metabolic disease, cardiovascular decline, sarcopenia, frailty, and loss of independence. The optimisation path leads to vitality, function, and independence well into your 70s and 80s.

What are you going to choose?

 

A Note on Women’s Hormonal Health

If you’ve used our main Triage Health Calculator, you’ll have noticed that it includes several menstrual and hormonal markers specifically for women. These are important health indicators, and I’ve included extensive guidance on what optimal ranges look like and how to interpret them.

However, you won’t find these metrics in the Triage Health Trajectory Tool, and I want to be upfront about why: I simply can’t model them reliably across a 50-year lifespan. Unlike metrics like VO₂ max or body fat percentage, which follow relatively predictable trajectories based on lifestyle choices, women’s hormonal health follows a much more complex and individualised pattern that doesn’t lend itself to simple projection models.

 

The Menopause Problem

The most obvious issue is menopause. I have no way to predict when any individual woman will go through menopause. The average age is around 51, but the normal range spans from early 40s to late 50s. Some women experience early menopause in their 30s due to medical conditions, surgeries, or genetics. Others sail through to 55+ with regular cycles.

This creates a fundamental modelling problem. If I’m projecting your hormonal trajectory from age 30 to 80, do I assume menopause at 45? 50? 55? Each of those scenarios creates dramatically different hormone profiles, and there’s no way for me to know which applies to you without detailed family history, medical history, and even then it’s largely unpredictable.

 

The Complexity of Female Hormone Cycles

Even before menopause, women’s hormones don’t follow the simple, gradual trajectories that work for metrics like testosterone in men. Male testosterone declines relatively smoothly and predictably with age (barring specific health issues). Female hormones? That’s a completely different story.

Women’s sex hormones fluctuate dramatically within each menstrual cycle; estrogen and progesterone rise and fall in complex patterns across 28 days (or whatever your cycle length is). Then there are larger patterns: cycles can become more irregular in your late 30s and 40s as you approach perimenopause. Some women experience relatively stable cycles until menopause hits suddenly. Others have years of irregular cycles, changing hormone levels, and unpredictable patterns during perimenopause.

Overlaying lifestyle factors (natural, maintenance, or optimisation) on this already complex pattern? Well, I honestly don’t have the knowledge or data to model that accurately. Would optimisation delay menopause by a year or two through better body composition and reduced inflammation? Maybe, but the evidence is mixed. Would it make perimenopause symptoms milder? Probably, but by how much and through what mechanisms? I don’t have clear enough answers to build a responsible projection model.

 

What I Do Know (And What I Don’t)

Here’s what I can tell you with confidence:

  • Lifestyle absolutely affects female hormonal health. Body composition, stress levels, sleep quality, exercise patterns, and nutrition all influence cycle regularity, hormone production, symptom severity, and reproductive health.
  • Optimisation-level lifestyle tends to support healthier cycles. Women who maintain lean body composition, train regularly (but not excessively), sleep well, and manage stress typically have more regular cycles, fewer PMS symptoms, and easier transitions through perimenopause and menopause.
  • The general principles still apply. Even though I can’t model specific hormone trajectories, the lifestyle factors that optimise everything else in this calculator (metabolic health, cardiovascular fitness, body composition, inflammation) also support hormonal health.

What I can’t tell you:

  • When you’ll go through menopause
  • How your estrogen and progesterone levels will change year-to-year
  • How quickly you’ll transition through perimenopause
  • Whether lifestyle optimization will delay menopause by 6 months, 2 years, or not at all
  • Exactly how much optimisation will reduce symptoms during perimenopause/menopause

 

The Honest Limitation

I’m a health and fitness coach with extensive experience, and I have a degree in biochemistry and biomolecular science, but I’m not an endocrinologist or a women’s health specialist. Female reproductive hormones are complex systems that I don’t feel qualified to model across 50-year timespans with the same confidence I have for metabolic or fitness markers.

Could someone with more specialised knowledge build a better model? Possibly. But it would require:

  • Much more individualised data (family history of menopause age, current cycle characteristics, PCOS history, etc.)
  • Complex branching projections (different scenarios for menopause at 45 vs 50 vs 55)
  • Accounting for huge individual variability in hormone patterns
  • Detailed understanding of how lifestyle factors influence reproductive ageing

That’s beyond the scope of what this tool is designed to do, and honestly, beyond my area of expertise (or indeed my coding skills).

 

What You Should Take Away

If you’re a woman using this calculator, focus on the other metrics that are included. These metrics are just as important for women as for men, and the trajectories are similar (with a few sex-specific adjustments in the scoring bands).

Your hormonal health is important, and you should absolutely track and optimise it using the main Triage Health Calculator. But for long-term trajectory planning, focus on the metrics we can reliably model, knowing that optimising those will create a foundation that supports hormonal health even if we can’t project the specific hormonal trajectory.

And if you’re working with a doctor or women’s health specialist who has deeper insight into your individual hormonal patterns and family history, they may be able to give you more personalised guidance on what to expect as you age and how lifestyle choices might influence your specific trajectory.

Ultimately, I’d rather be honest about the limitations of the model than pretend I can reliably project something I can’t. The metrics included are ones I’m confident in. Women’s reproductive hormones across 50 years? That’s a level of complexity that requires specialised expertise I don’t have.

 

SUMMARY PATTERNS

Alright, we’ve walked through all the metrics in detail. Now let’s zoom out and look at the patterns. Because once you see how these metrics behave across the board, you’ll understand exactly what you’re dealing with and what’s actually possible.

 

Metrics that IMPROVE initially with optimisation:

This is the good news is that many metrics don’t just slow their decline with optimisation, they actually get better than your baseline when you first start taking your health seriously. Here’s the breakdown:

 

Large improvements (>20%): ApoB, LDL, Triglycerides, hs-CRP, ALT/AST (all -20% to -40%)

These are your cardiovascular and metabolic markers that respond dramatically to lifestyle intervention. We’re talking about 20-40% reductions in the first year or two. Why such massive changes? Because these markers are highly responsive to things like:

  • Weight loss (especially visceral fat loss)
  • Dietary improvements (cutting refined carbs, increasing fibre, reducing saturated fat)
  • Exercise (both cardio and resistance training improves lipid profile)
  • Reduced inflammation (from all of the above)

If your ApoB is 1.0 g/L and you get serious about optimisation, you can realistically drop it to 0.6-0.8 g/L within a year. If your triglycerides are 2.0 mmol/L, you can get them down to 1.2-1.4 mmol/L. These aren’t theoretical projections; I’ve seen these changes hundreds of times in real clients.

 

Moderate improvements (10-15%): HDL, Glucose, HbA1c, Testosterone (all +10% to +15%)

These metrics improve, but more modestly. HDL increases with regular exercise (especially cardio). Glucose and HbA1c improve with weight loss, increased muscle mass, and better insulin sensitivity. Testosterone in men responds to resistance training, sleep optimisation, stress management, and healthy body composition.

A 10-15% improvement might not sound like much, but it’s often the difference between average and optimal ranges. Going from 1.3 mmol/L HDL to 1.5 mmol/L (15% increase) moves you from good to optimal cardiovascular protection.

 

Strength gains (20-40%): All strength metrics can improve 20-40% in the first 1-3 years

This is where optimisation really shines. If you’ve never trained seriously, you’re nowhere near your genetic potential for strength. Start a proper resistance training program, and you can see:

  • 25-30% squat improvement
  • 30-40% deadlift improvement
  • 20-25% bench press improvement
  • 40%+ chin-up improvement (from 10 reps to 14+ reps)

These “newbie gains” happen because you’re tapping into untrained potential. Your nervous system learns to recruit muscle fibres more efficiently, you build new muscle tissue, and your technique improves. It’s not uncommon for a 40-year-old who’s never trained to make strength gains that look like a 20-year-old athlete in their first 1-2 years of training.

 

Body comp improvements (8-12%): Body fat, waist, and BMI can drop 8-12% initially

Aggressive fat loss combined with muscle maintenance/building through resistance training can produce dramatic body composition changes. Dropping from 20% body fat to 17-18% (about a 12% reduction), losing 10 cm off your waist, and dropping your BMI from 27 to 24. All of this is achievable in 1-2 years with dedicated effort.

The key word here is “initial”; these improvements happen in the first 1-3 years when you first get serious about optimisation. After that, you shift into maintenance mode, holding onto those improved levels.

 

Metrics that DECLINE regardless (but optimisation slows it):

Now for the reality check: some metrics are going to decline no matter what you do. That’s actual biological ageing, not just lifestyle-driven decline. The question is: how fast do they decline?

 

VO₂ Max: Declines at all ages, optimisation just slows it significantly

Even elite endurance athletes lose VO₂ max with age. It’s unavoidable; your maximum heart rate declines, your cardiovascular system becomes less efficient, and cellular respiration capacity diminishes. But the rate matters enormously. Natural decline: 0.5-3% per year. Optimisation: 0.2-0.6% per year. Over 50 years, that’s the difference between a 53% loss versus a 16% loss.

 

HRV: Can improve initially, but must decline with ageing (autonomic system)

Your autonomic nervous system becomes less flexible with age; that’s biological reality. You can improve HRV initially through training, sleep, and stress management, but eventually it will decline. Optimisation slows that decline dramatically, keeping you in good ranges when the natural trajectory would put you in average/poor ranges.

 

eGFR: Kidney function declines with age, optimisation slows it

You lose nephrons (kidney filtering units) as you age; there’s no reversing that. But you can slow the rate of loss dramatically by controlling blood pressure, maintaining excellent blood sugar control, staying hydrated, and avoiding nephrotoxic substances. Natural decline: 28% over 50 years. Optimisation: 6% over 50 years.

 

FFMI: Muscle loss (sarcopenia) is inevitable, optimisation delays/reduces it

Even lifelong athletes lose some muscle mass with age. Hormone production declines, protein synthesis becomes less efficient, and recovery slows. But sedentary people lose 25% of their muscle mass by age 80, while those who optimise lose maybe 5-10%. That’s the difference between frailty and functionality.

 

Strength: Will decline eventually, but optimisation delays it 20-30 years

You can’t maintain peak strength forever. But you can delay serious strength decline by decades. Natural trajectory: starts declining in your 30s, accelerates in 50s-60s, catastrophic by 70s-80s. Optimisation trajectory: maintain or improve until 50s, very slow decline in 60s-70s, still functional in 80s.

 

Testosterone (men): Will decline after 35, optimisation just slows the decline

Your testes produce less testosterone as you age; that’s biology. But lifestyle massively influences the rate. Natural decline: 39% over 50 years, ending in low-normal range. Optimisation: 18% over 50 years, staying in the optimal range.

 

Metrics where optimisation = ZERO change after initial boost:

This is fascinating: some metrics improve dramatically with optimisation, then just… stay there. No ongoing decline. Flat lines for decades.

 

Lipids: Stay at optimised level indefinitely (ApoB, LDL, Triglycerides)

Once you’ve optimised your diet, body composition, and exercise habits, your lipid markers stabilise at those improved levels. There’s no biological ageing process that forces your cholesterol to rise. The natural trajectory shows rising lipids because people gain weight, become more sedentary, and eat progressively worse. Remove those factors, and your lipids stay excellent.

 

Metabolic: Stay at optimised level (Glucose, HbA1c, Liver enzymes)

Same story. There’s no biological law that says your fasting glucose must rise with age. It rises because people become progressively more insulin-resistant due to weight gain, inactivity, and poor diet. Maintain excellent insulin sensitivity through training, lean body mass, and good nutrition, and your metabolic markers stay locked in the optimal range indefinitely.

 

Inflammation: Stays low (hs-CRP)

Chronic inflammation isn’t an inevitable part of ageing; it’s a consequence of obesity, sedentary behaviour, poor diet, and chronic stress. Remove those inflammatory stimuli through optimisation, and inflammation stays low. You can have the inflammatory profile of a 25-year-old at age 75.

 

Sleep: Stays optimised

Once you’ve established excellent sleep habits and prioritised 8+ hours per night, there’s no biological reason that needs to change. Sleep duration is relatively stable with optimisation (though sleep architecture and quality may shift slightly with age, which this metric doesn’t capture).

 

KEY TAKEAWAYS

Let me distil everything we’ve covered into the insights that actually matter for your decision-making:

 

1. Cardiovascular disease is the biggest threat

Before we talk about anything else, let’s be brutally honest about what actually kills most people: heart disease and stroke. Cardiovascular disease is the leading cause of death globally, accounting for roughly 1 in 3 deaths, and the critical thing most people don’t understand is that the risk is cumulative.

Look at those ApoB, LDL, and triglyceride trajectories. The natural path shows your cholesterol markers steadily worsening year after year. This isn’t just about where you end up at age 80; it’s about how many years you spend with elevated lipids accumulating damage in your arteries.

Every year you spend with high ApoB or LDL is another year of cholesterol particles infiltrating your arterial walls, oxidising, triggering inflammation, and building up atherosclerotic plaques. This process starts in your 20s and 30s, even if you feel perfectly healthy. By the time you’re 50 or 60, you may have accumulated 20-30 years of arterial damage.

The natural trajectory shows ApoB rising from 0.8 g/L at age 30 to 1.35 g/L by age 80. That’s 50 years of progressively worsening cardiovascular risk, with the last 30+ years spent well above optimal levels. That’s 30+ years of cumulative arterial damage.

With the optimisation trajectory, you actually reduce ApoB to 0.68 g/L initially, then hold steady around 0.72 g/L for the next 50 years. You spend your entire adult life in the optimal range, accumulating minimal arterial damage.

This is why starting early matters so much for cardiovascular health specifically. If you optimise in your 20s or 30s and maintain low lipids for life, you might reach age 70 with arteries that are relatively clean. If you follow the natural trajectory until 50, then try to optimise, you’ve already got 20+ years of plaque buildup that’s much harder to reverse.

Ideally, you want to keep those lipid markers in the optimal range for as many years of your life as possible. Every year at optimal levels is a year you’re not accumulating arterial damage. This is your most important long-term health metric.

 

2. Metabolic disease is still a major threat (but more reversible)

Now, that said, metabolic disease is also a huge deal. Look at those glucose, HbA1c, and liver enzyme trajectories. The natural path takes you straight into pre-diabetic/diabetic territory and fatty liver disease. This is because we live in an obesogenic world. Ultra-processed foods, massive portions, constant snacking, sedentary jobs, and poor sleep. The modern environment is engineered to make you metabolically unhealthy.

But the critical difference from cardiovascular disease is that metabolic disease is more reversible. Fatty liver can often be completely reversed with weight loss. Pre-diabetes can be reversed. Even early-stage type 2 diabetes can sometimes be reversed with aggressive lifestyle intervention.

And those 12-15% initial improvements in glucose and HbA1c? Those happen fast when you lose weight, start training, and clean up your diet. Within 3-6 months, you can reverse years of metabolic damage. It’s not cumulative in the same way cardiovascular disease is – you can actually hit the reset button on metabolic health to a large degree.

That doesn’t make it less important, but it does mean the timeline is different. Cardiovascular disease requires lifelong attention to prevent cumulative damage. Metabolic disease requires urgent attention when it develops, but responds more quickly to intervention.

 

3. Body composition spirals

All four fat-related metrics (body fat %, waist circumference, BMI, WHtR) show the same pattern: roughly 23% increase over 50 years on the natural trajectory. You go from lean to overweight to obese. And it’s insidious; gaining 0.3-0.5% body fat per year doesn’t feel like much. You don’t notice it year-to-year. But compound that for 30 years and suddenly you’re 15-20 pounds heavier with 8-10% more body fat.

The spiral works both ways though. Lose fat, build muscle, and maintain it through optimisation, and you end up leaner and potentially even more muscular at 80 than you were at 30. The compound effect works in your favour when you make it work for you.

 

4. Strength loss is catastrophic

50-85% loss of strength by age 80 without intervention. You lose more than half your strength, and for upper body metrics like bench press and chin-ups, you lose up to 85%. That’s the difference between independence and needing assistance with daily activities.

But optimisation prevents almost all of it. You can maintain strength levels at 80 that match or exceed where you were at 30. This is one of the most actionable, high-impact interventions you can make.

 

5. Cardiovascular fitness decline is severe

VO₂ Max drops 53% naturally (45 → 21 ml/kg/min). This isn’t just awful for athletic performance; it’s also awful for mortality risk. VO₂ max is one of the single strongest predictors of longevity we have. Dropping into the “poor” range (below 25-30 ml/kg/min) increases your mortality risk by 4-5x compared to maintaining “good” or “excellent” ranges.

Optimisation keeps you in the good range at 80 (43.5 ml/kg/min), giving you the cardiovascular fitness of someone 25-30 years younger. That’s 8-12 extra years of life expectancy based on the research.

 

6. Optimisation genuinely works

This isn’t wishful thinking or exaggeration. The data is clear that optimisation can prevent or reverse almost all decline in the first 1-3 years, then maintain excellent levels. We’re seeing 20-40% improvements in many metrics, complete prevention of decline in others, and dramatic slowing of decline in metrics that must decline with age.

This is real. This is achievable. I’ve seen it hundreds of times in real people, and the scientific literature supports every trajectory in this calculator.

 

7. The compounding effect is HUGE

This is the insight that should fundamentally change how you think about daily choices. Small annual % changes compound to massive differences over 50 years.

A 1% annual increase in a metabolic marker sounds trivial. But compound that for 40 years and you’ve increased by 49%. A 0.5% annual decline in VO₂ max sounds manageable. Compound it for 50 years and you’ve lost 22%.

Conversely, improving a metric by 25% initially and then maintaining it flat for 50 years? That’s the difference between disease and health, between frailty and vitality.

Every workout you do or skip, every meal choice, every night of good or poor sleep are data points in a trajectory that compounds over decades.

 

8. Starting early matters

The biggest optimisation gains happen in the 20s-40s age range. This is compound interest for your health, just like saving for your pension. The earlier you start, the more time you have for improvements to compound, and the longer you maintain optimal ranges before any age-related decline begins.

If you’re 25 and start optimising now, you can maintain optimal ranges until your 50s or 60s before you see any meaningful decline. If you wait until 45 to start, you can still make dramatic improvements, but you’ve “lost” 20 years of compounding benefits.

And for cardiovascular health specifically, those early years matter enormously because of cumulative arterial damage. Starting at 25 versus starting at 45 could mean the difference between 20 years of plaque accumulation versus starting with relatively clean arteries.

 

9. But it’s never too late

The flip side is that optimisation benefits at ANY age. Even if you’re 55, 65, or 75 and have followed the natural trajectory up until now, you can still make dramatic improvements and slow further decline.

However, it’s harder to achieve large gains the older you are. A 60-year-old isn’t going to improve VO₂ max by 15% like a 30-year-old might. But you can still improve, and more importantly, you can prevent the continued catastrophic decline that the natural trajectory shows.

Starting at 50 and following the optimisation trajectory for 30 years is infinitely better than following the natural trajectory for those same 30 years. You’re not “too late”, you’re just deciding whether the next 30 years will follow the red line or the green line.

 

10. You’re Not Choosing Between Effort and No Effort, You’re Choosing Between Different Types of Suffering

Ultimately, you’re not choosing between “working hard on your health” and “living an easy life.” You’re choosing between different types and timings of suffering. Seneca, the Stoic philosopher, wrote: “We suffer more in imagination than in reality.” He also wrote: “It is not that we have a short time to live, but that we waste a lot of it.”

The optimisation trajectory requires effort now: 5 hours per week training, conscious food choices, prioritising sleep, and managing stress. That’s real effort. That’s a real sacrifice of immediate comfort.

But the natural trajectory requires suffering later: years or decades of chronic disease, medications with side effects, physical limitations, loss of independence, and watching others live actively while you sit on the sidelines. That’s also real suffering. Often, much worse suffering.

You’re not choosing effort versus no effort. You’re choosing short-term discomfort versus long-term suffering. Effectively, you’re choosing whether to pay the mortgage (regular training) or default and face foreclosure (disease and frailty). The foreclosure is always more expensive than the mortgage payments, but the mortgage payments happen every month, while foreclosure feels distant and abstract.

Sartre wrote that we are “condemned to be free”, and we cannot escape the responsibility of choosing. Every day you don’t train is a choice. Every meal is a choice. Pretending you’re “too busy” or “too tired” or “too old” is what Sartre called “bad faith”. Denying your own agency and pretending you don’t have a choice when you absolutely do.

The trajectories make this undeniable: you are choosing. The only question is whether you’re choosing consciously or unconsciously, whether you’re choosing the short-term discomfort of optimisation or the long-term suffering of decline.

Neither path is easy. But one preserves agency, capacity, and independence. The other slowly surrenders all three. You must choose your suffering wisely.

 

The Bottom Line

These trajectory rates, projections, and patterns all point to the same fundamental truth: your health outcomes are largely determined by your daily choices, compounded over time.

The natural trajectory (the one that 70-80% of the population follows) leads to cardiovascular disease (from cumulative arterial damage), metabolic disease, sarcopenia, frailty, and loss of independence. It’s not subtle. It’s not minor. It’s catastrophic.

The optimisation trajectory leads to maintaining excellent health markers, physical function, and independence well into your 70s and 80s. You end up with the cardiovascular health, metabolic health, strength, and body composition of someone decades younger.

The maintenance trajectory splits the difference; you slow decline significantly without requiring elite-level commitment.

You now have the data. You can see exactly where each path leads. What are you going to do with this information?

 

Health Optimisation

Now, I have noted the health optimisation scenario throughout this article, and I just want to very quickly provide you with a very brief snapshot of the kinds of things that would be required for health optimisation for each health metric. This is just going to be brief, as this is not the main point of this article, and I intend to write much more comprehensive articles on each of these in future (subscribe to our newsletter to stay up to date).

The “do nothing” option is fairly straightforward, as is the “do the bare minimum”. Most people are aware that they should be eating well, exercising regularly (at least hitting the minimum guidelines), managing their stress, and sleeping ~8 hours a night. This is the bare minimum, and as you can see from the trajectories, it does actually do a lot of good.

However, you can optimise things even further.

 

Before We Dive Into Strategies: Understanding Behaviour Change

The strategies that follow are evidence-based and effective. But knowing what to do and actually doing it are completely different problems. You probably already know you should exercise, eat well, sleep adequately, and manage stress. The issue isn’t information; it’s implementation. So before we get into the specific strategies, let me give you some of the psychological frameworks that make implementation possible.

 

Implementation Intentions 

Research shows that “if-then” planning significantly increases follow-through. Don’t just decide to “optimise” or “work out more.” Get specific:

  • “If it’s Monday, Wednesday, or Friday at 6:00 AM, then I train for 60 minutes.”
  • “If I’m at a restaurant, then I order protein and vegetables first, then consider adding carbs.”
  • “If it’s 9:00 PM, then I begin my sleep routine regardless of what’s happening.”

The “if-then” structure bypasses the decision-making moment where most people fail. You’re not deciding whether to work out each morning; you’ve already decided. You’re just executing the predetermined plan.

 

Habit Stacking 

New behaviours are easier to adopt when attached to existing behaviours. BJ Fogg calls this “anchoring.” Examples:

  • “After I pour my morning coffee, I take my vitamins.”
  • “After I finish lunch, I go for a 10-minute walk.”
  • “After I brush my teeth at night, I prepare my gym clothes for the morning.”

You’re using existing habits as triggers for new habits, making them automatic rather than requiring willpower each time.

 

The Minimum Viable Dose

Most people fail because they try to go from 0 to optimisation overnight. They commit to training 6x/week, overhauling their entire diet, sleeping 9 hours, and meditating daily. They last two weeks, then crash.

Start with maintenance: 2-3 workouts per week, adding protein to each meal, and getting 7 hours of sleep consistently. Master that for three months. Then add. The compound effect works on habit formation too: small habits, sustained, beat heroic efforts abandoned.

 

Identity-Based Change 

Don’t say “I’m trying to work out more.” Say “I’m someone who trains.” Don’t say “I should eat better.” Say “I’m someone who eats whole foods.”

The identity shift changes the question from “should I work out today?” (decision fatigue) to “would someone like me skip training?” (identity reinforcement). You’re not forcing behaviour through willpower, you’re acting consistently with your identity.

 

Environment Design Over Willpower

Your environment is stronger than your willpower. I is much easier if you don’t try to resist temptation, and instead remove it. Don’t try to force yourself to train; make training the default. You can do this a number of ways, including:

  • Gym clothes laid out the night before
  • Healthy food prepped and visible
  • Tempting foods removed from the house (or at least not easily accessible and visible)
  • Training partners scheduled (social commitment)
  • Calendar blocked for workouts (treated like meetings)
  • Gym located en route to work, not 20 minutes away

If you make the “right” choice the easy choice, and make the “wrong” choice require effort, you are much more likely to stick to your plan. 

 

The “Never Zero” Principle

Can’t do your full workout? Do 10 minutes. Can’t hit your protein target perfectly? Get close. Can’t sleep 8 hours? Get 7. Never zero.

The habit matters more than the volume. Never zero keeps the neural pathway active, prevents the spiral of “I already missed today, might as well miss the week.”

 

Now, with those frameworks in mind, let’s look at the specific strategies for each metric… The following are scientifically-backed interventions to optimise each health metric tracked in the Triage Health Trajectory Tool, plus critical factors to avoid that negatively impact these markers.

 

Cardiovascular Markers

ApoB (Apolipoprotein B)

OPTIMISE (Lower is Better):

  • Dietary fibre (30-40g/day): Soluble fibre binds bile acids, forcing cholesterol excretion. Viscous fibres (oats, psyllium, beans) are most effective
  • Statins (when indicated): 30-55% reduction is typical. Most evidence-based pharmaceutical intervention for reducing ApoB.
  • Plant sterols/stanols (2-3g/day): Block intestinal cholesterol absorption, ~10% reduction.
  • Regular aerobic exercise (150+ min/week moderate intensity): Increases LDL receptor activity, enhances particle clearance.
  • Weight loss (if overweight): 5-10% body weight loss → ~5-8% ApoB reduction.
  • Limit saturated fat (<7-10% of calories): Replace with unsaturated fats, particularly MUFA/PUFA.
  • Omega-3 fatty acids (EPA/DHA 2-4g/day): Modest effect on ApoB, stronger on triglycerides.
  • Bergamot extract (500-1000mg/day): Emerging evidence for ~15-25% LDL reduction via HMG-CoA reductase inhibition.
  • PCSK9 inhibitors (if very high risk): 50-60% reductions possible but expensive.
  • Ezetimibe (10mg/day): Blocks cholesterol absorption, ~15-20% additional reduction when combined with statins.

AVOID (Things That Increase ApoB):

  • Trans fats (partially hydrogenated oils): Strongly increases ApoB, are inflammatory, and there is no safe level.
  • Excess saturated fat (>10% calories): From fatty meats, butter, tropical oils, and full-fat dairy.
  • High refined carbohydrate intake: White bread, sugary drinks → triglyceride → VLDL → ApoB conversion
  • Sedentary lifestyle: <30 min activity/day associated with 15-25% higher ApoB.
  • Excess alcohol (>2 drinks/day): Increases hepatic VLDL production.
  • Smoking: 10-15% higher ApoB levels, oxidises particles making them more atherogenic.
  • Chronic stress/poor sleep: Elevates cortisol → increased hepatic lipoprotein synthesis.
  • Anabolic steroids: Can increase ApoB 20-40% while lowering HDL.

 

LDL-C (LDL Cholesterol)

OPTIMISE (Lower is Better):

  • Statins (atorvastatin, rosuvastatin): Gold standard, 30-55% reductions.
  • Dietary pattern shift: Mediterranean or Portfolio diet patterns show 20-35% reductions.
  • Soluble fibre (10-25g/day): Psyllium husk is particularly effective (~5-10% reduction per 10g).
  • Plant sterols (2g/day minimum): Fortified foods or supplements.
  • Reduce saturated fat: Replace with MUFA (olive oil, avocados, nuts) and PUFA (fatty fish, flaxseed).
  • Soy protein (25g/day): Modest 3-5% reduction when replacing animal protein.
  • Regular cardio exercise: 150-300 min/week, moderate intensity.
  • Maintain healthy weight: Each 10kg weight loss → ~0.13 mmol/L (~5mg/dL) LDL reduction
  • Green tea (3-5 cups/day): Catechins may reduce LDL ~2-6 mg/dL.
  • Garlic extract (aged, 600-1200mg/day): Small but measurable reductions (5-8%).
  • Red yeast rice: Contains natural statins (monacolin K), 15-25% reductions, but quality varies.

AVOID (Things That Increase LDL-C):

  • Trans fats: Most potent dietary factor, raises LDL while lowering HDL
  • Excess saturated fat: Palm oil, coconut oil, fatty meats, butter, and cheese.
  • High sugar intake: Particularly fructose, drives hepatic lipogenesis.
  • Smoking: Direct oxidative damage to LDL particles plus 7-10% elevation.
  • Excess dietary cholesterol: Less impactful than once thought but still relevant (>300mg/day).
  • Hypothyroidism: Uncontrolled low thyroid → 20-40% LDL elevation.
  • Chronic kidney disease: Impaired clearance mechanisms.
  • Certain medications: Beta blockers, thiazide diuretics, corticosteroids, some immunosuppressants.

 

Triglycerides

OPTIMISE (Lower is Better):

  • Reduce refined carbohydrates: The single most effective dietary intervention, especially fructose/sucrose.
  • Omega-3 fatty acids (EPA/DHA 2-4g/day): 20-30% reductions, strongest evidence for high-dose EPA.
  • Weight loss: 5-10% body weight → 20-30% triglyceride reduction.
  • Limit alcohol: Even moderate intake elevates TG; abstinence if >200mg/dL.
  • Regular exercise (cardio + resistance): 20-30% reductions with consistent training.
  • Low-carb or ketogenic diet: Can reduce TG 30-50% in insulin-resistant individuals.
  • Increase fibre intake: Particularly viscous/soluble types.
  • Niacin (1-2g/day extended-release): 20-30% reduction, but tolerance/side effects common.
  • Fenofibrate (if very high): 30-50% reductions, particularly useful if TG >500mg/dL.
  • Time-restricted eating: 12-16 hour daily fast may improve TG metabolism 10-20%.
  • Intermittent fasting: Alternate day or 5:2 protocols show 15-25% improvements.
  • Avoid or limit fructose: High fructose corn syrup, agave, fruit juice concentrates.

AVOID (Things That Increase Triglycerides):

  • Refined carbohydrates & sugar: White bread, pasta, rice, sweets, sugary beverages (strongest dietary factor).
  • Excess alcohol: Especially beer and mixed drinks, even moderate intake is problematic if TG are elevated.
  • Excess caloric intake: Chronic positive energy balance → hepatic lipogenesis.
  • Sedentary lifestyle: Strong dose-response relationship with TG levels.
  • Trans fats: Worsen TG, along with other lipid parameters.
  • High fructose intake: Uniquely lipogenic, bypasses glycolytic regulation.
  • Oral estrogens: Can significantly elevate TG (transdermal forms are less problematic).
  • Beta blockers: Particularly non-selective types can increase TG 20-50%.
  • Thiazide diuretics: Modest TG elevation (10-15%).
  • Corticosteroids: Dose-dependent increases.
  • Uncontrolled diabetes: Insulin deficiency/resistance → impaired lipoprotein lipase activity.
  • Fruit juice: Even “natural” juice is fructose-dense without fibre benefit.

 

HDL Cholesterol (Higher is Better, But Optimal Range Exists)

OPTIMISE (Raise HDL Within Optimal Range):

  • Regular aerobic exercise: A fairly reliable way to raise HDL, 5-10% increase with 150+ min/week.
  • Weight loss (if overweight): 5-10% weight loss → 10-15% HDL increase typically.
  • Moderate alcohol (1-2 drinks/day): Raises HDL 10-15% BUT increases other risks, not recommended as primary intervention.
  • Quit smoking: Can increase HDL 5-10mg/dL within weeks.
  • Monounsaturated fats: Replace saturated/trans fats with olive oil, avocados, nuts.
  • Niacin (1-2g/day): 15-35% HDL increases, but recent trials question cardiovascular benefit.
  • Omega-3 fatty acids: Modest effect on HDL (3-5% increase).
  • Purple/red produce: Anthocyanins may modestly boost HDL.
  • Reduce refined carbs: Very low-fat diets can lower HDL; moderate fat intake is better.
  • Strength training: Combined with cardio shows additive HDL benefits.
  • Adequate sleep (7-9 hours): Sleep deprivation is associated with 5-10% lower HDL.
  • Manage stress: Chronic stress/cortisol suppresses HDL.

AVOID (Things That Lower HDL):

  • Smoking: One of the most powerful HDL suppressor, 10-15% reduction.
  • Trans fats: Uniquely lowers HDL while raising LDL (double harm).
  • Very low-fat diets (<15% calories from fat): Can drop HDL 10-20%.
  • High refined carbohydrate intake: Particularly when replacing healthy fats.
  • Sedentary lifestyle: Strong inverse relationship with HDL.
  • Obesity/excess visceral fat: Especially android (abdominal) obesity.
  • Anabolic steroids: Can crash HDL 30-70%, severe cardiovascular risk.
  • Beta blockers: Particularly non-selective types, 10-15% reduction.
  • Benzodiazepines: Chronic use is associated with lower HDL.
  • Uncontrolled diabetes: Poor glycemic control impairs HDL metabolism.
  • Hypertriglyceridemia: High TG inversely correlates with HDL.

 

Blood Pressure (Systolic & Diastolic)

OPTIMISE (Lower is Better, But Optimal Range Exists):

  • DASH diet: Dietary Approaches to Stop Hypertension, 8-14 mmHg systolic reduction.
  • Reduce sodium (<1500-2300mg/day): 5-6 mmHg reduction per 1000mg reduction.
  • Increase potassium (3500-4700mg/day): From food sources, 4-5 mmHg reduction.
  • Weight loss: Each 1kg lost → ~1 mmHg reduction in systolic BP.
  • Regular aerobic exercise (150+ min/week): 5-8 mmHg reduction in hypertensive individuals.
  • Limit alcohol (≤1-2 drinks/day): Excess alcohol major BP driver.
  • Beetroot juice/nitrate-rich foods: 4-10 mmHg reductions via NO pathway.
  • Magnesium supplementation (300-500mg/day): 2-5 mmHg reduction if deficient.
  • Garlic extract (600-1200mg/day): 8-10 mmHg reductions in some studies.
  • CoQ10 (100-200mg/day): ~3-5 mmHg reductions in hypertensive patients.
  • Meditation/stress reduction: Regular practice → 5-10 mmHg reductions.
  • Adequate sleep (7-9 hours): Sleep debt is strongly associated with hypertension.
  • Hibiscus tea (3 cups/day): Comparable to some BP medications in trials.
  • Omega-3 fatty acids (2-3g/day): Modest 2-3 mmHg reductions.
  • Reduce caffeine (if sensitive): Can raise BP 5-10 mmHg acutely.

AVOID (Things That Increase Blood Pressure):

  • Excess sodium intake: Particularly if salt-sensitive (>2300mg/day).
  • Excess alcohol: >2 drinks/day progressively increases BP.
  • Sedentary lifestyle: Strong dose-response with sitting time.
  • Chronic stress/anxiety: Sustained cortisol elevation.
  • Poor sleep quality/quantity: <6 hours associated with hypertension risk.
  • Obesity: Particularly visceral adiposity, 1-2 mmHg per BMI point above 25.
  • Smoking: Acute 5-10 mmHg increase per cigarette, chronic vascular damage.
  • NSAIDs: Ibuprofen, naproxen can increase BP 5-10 mmHg with chronic use.
  • Decongestants: Pseudoephedrine and phenylephrine both elevate BP
  • Liquorice/glycyrrhizin: Mimics aldosterone, fluid retention.
  • Excess caffeine: >400mg/day if sensitive (varies widely by individual)
  • Oral contraceptives: Can modestly elevate BP in some women
  • Corticosteroids: Dose-dependent BP elevation
  • SNRIs/some antidepressants: Venlafaxine and others can raise BP
  • Energy drinks: The combination of caffeine, sugar, and stimulants.

 

Metabolic Markers

Fasting Glucose

OPTIMISE (Lower is Better):

  • Weight loss (if overweight): 5-10% weight loss → 20-30% improvement in insulin sensitivity.
  • Regular exercise: Both cardio (150+ min/week) and resistance training (2-3x/week) – 10-20% glucose reduction.
  • Low-glycemic diet: Emphasise vegetables, legumes, and whole grains; avoid refined carbs.
  • Increase fibre (25-38g/day): Particularly viscous/soluble fibre, as this slows glucose absorption.
  • Time-restricted eating: 12-16 hour daily fast can improve insulin sensitivity 10-30%.
  • Low-carb or ketogenic diet: Can reduce glucose 10-20% in insulin-resistant individuals.
  • Cinnamon (1-6g/day): May improve glucose 10-15% in some individuals.
  • Berberine (500mg 3x/day): Comparable to metformin in some trials, 15-20% reductions.
  • Alpha-lipoic acid (600mg/day): Improves insulin sensitivity.
  • Chromium picolinate (200-1000mcg/day): If deficient, modest glucose improvements.
  • Magnesium (300-400mg/day): Cofactor in glucose metabolism, 5-10% improvement if deficient.
  • Vinegar with meals: 2 tbsp before high-carb meals reduces glucose spike 20-30%.
  • Adequate sleep (7-9 hours): Sleep deprivation increases insulin resistance by 25-30%.
  • Strength training: Increases muscle GLUT4, improves glucose disposal.
  • Metformin (if prediabetic/indicated): 500-2000mg/day, can prevent progression to diabetes.

AVOID (Things That Increase Glucose):

  • Refined carbohydrates: White bread, pasta, white rice, and sugary foods/beverages.
  • Sugary beverages: Soda, fruit juice, and sweetened coffee drinks lead to rapid glucose spikes.
  • Sedentary lifestyle: Sitting >8 hours/day is strongly associated with insulin resistance.
  • Excess caloric intake: Chronic overfeeding → insulin resistance.
  • Trans fats: Impair insulin signalling atthe  cellular level.
  • Sleep deprivation: <6 hours → acute 25-40% reduction in insulin sensitivity.
  • Chronic stress: Elevated cortisol drives gluconeogenesis, impairs insulin action.
  • Excess alcohol: Especially beer and mixed drinks with sugar.
  • Smoking: 30-40% increased risk of insulin resistance.
  • Corticosteroids: Directly increase glucose production and reduce insulin sensitivity.
  • Certain medications: Atypical antipsychotics, some HIV medications, tacrolimus.
  • High fructose intake: Particularly problematic for hepatic insulin resistance.
  • Skipping breakfast: Associated with worse glucose control throughout day.
  • Large evening meals: Glucose tolerance is worse later in day due to circadian rhythm.

 

HbA1c (Glycated Haemoglobin)

OPTIMISE (Lower is Better):

  • Consistent glucose control: All glucose-lowering strategies apply (see Fasting Glucose section).
  • Weight loss: 5-10% reduction → 0.5-1.0% HbA1c improvement.
  • Regular exercise: Combined cardio + resistance → 0.6-0.8% HbA1c reduction.
  • Low-carb/ketogenic diet: 0.5-1.5% reductions in diabetics/prediabetics.
  • Continuous glucose monitoring: Awareness drives behavioural change → 0.3-0.5% improvement.
  • Metformin (if indicated): 1-1.5% reduction typically.
  • GLP-1 agonists (if diabetic): Semaglutide, liraglutide → 1-2% reductions.
  • SGLT2 inhibitors (if diabetic): Empagliflozin, dapagliflozin → 0.5-1% reductions.
  • Berberine (1500mg/day divided): 0.5-1% reductions in some studies.
  • Time-restricted eating: 0.3-0.5% reductions via improved insulin sensitivity.
  • Adequate sleep (7-9 hours): Critical for glucose regulation.
  • Stress management: Meditation, yoga → improved glycemic control.
  • Avoid glucose variability: Stable glucose is better than the same average with high peaks/valleys.

AVOID (Things That Increase HbA1c):

  • All factors that raise glucose (see Fasting Glucose section)
  • Iron deficiency: Can falsely elevate HbA1c (shortened RBC lifespan)
  • Vitamin B12/folate deficiency: Can affect HbA1c measurement
  • Chronic kidney disease: Uremia affects RBC turnover and glycation
  • Certain haemoglobin variants: HbS, HbC, HbE can interfere with measurement
  • Recent blood transfusions: Will temporarily affect HbA1c accuracy

 

ALT & AST (Liver Enzymes)

OPTIMISE (Lower is Better):

  • Weight loss: Single most effective intervention for NAFLD, 5-10% → 30-50% enzyme reduction.
  • Regular exercise: 150+ min/week, and particularly HIIT, shows 20-40% reductions.
  • Mediterranean diet: Anti-inflammatory pattern, rich in MUFA, shown to reverse NAFLD.
  • Reduce fructose/added sugars: Particularly high-fructose corn syrup, the most hepatotoxic sugar.
  • Reduce saturated fat intake: Replace with MUFA/PUFA sources.
  • Coffee consumption: 2-4 cups/day associated with 20-30% lower ALT/AST (hepatoprotective).
  • Omega-3 fatty acids (2-4g/day EPA/DHA): Reduces hepatic fat accumulation 20-40%.
  • Vitamin E (800 IU/day): In non-diabetic NASH, can reduce ALT 30-40%.
  • Resistance training: Builds muscle, improves insulin sensitivity, and reduces hepatic fat.
  • Limit alcohol: Abstinence if elevated enzymes; safe limits debated, but <1 drink/day generally can be OK if no liver disease.
  • Adequate sleep: Poor sleep is associated with NAFLD progression.
  • Avoid rapid weight loss: Gradual 0.5-1kg/week is better than crash diets (can temporarily worsen ALT).
  • Silymarin (milk thistle): 140mg 3x/day shows modest hepatoprotective effects.
  • Green tea extract: EGCG may reduce hepatic fat, but use cautiously (rare hepatotoxicity).

AVOID (Things That Increase ALT/AST):

  • Excess alcohol: Even moderate intake if already elevated.
  • Fructose/high-fructose corn syrup: Uniquely lipogenic to the liver.
  • Sugary beverages: Direct hepatotoxicity via fructose + glucose combination.
  • Excess saturated fat: Particularly problematic for NAFLD.
  • Obesity: Visceral adiposity strongly linked to NAFLD/NASH.
  • Sedentary lifestyle: An independent risk factor for hepatic steatosis.
  • Rapid weight loss: Paradoxically can worsen the enzymes short term.
  • Hepatotoxic supplements: Some bodybuilding supplements, kava, and certain herbals.
  • Acetaminophen overuse: Even therapeutic doses with alcohol or in liver disease.
  • Statins: Can elevate enzymes 1-3% (usually benign, monitor).
  • Anabolic steroids: Severe hepatotoxicity, enzyme elevations 2-10x normal.
  • Certain medications: Isoniazid, methotrexate, amiodarone, antiretrovirals, and some antifungals.
  • Uncontrolled diabetes: Hyperglycemia promotes hepatic fat accumulation.
  • Trans fats: Inflammatory and lipogenic to the liver.

 

Inflammatory, Kidney & Thyroid Markers

hs-CRP (High-Sensitivity C-Reactive Protein)

OPTIMISE (Lower is Better):

  • Weight loss: 5-10% weight loss → 20-40% CRP reduction.
  • Regular exercise: Both cardio and resistance, 30-40% reductions with consistent training.
  • Anti-inflammatory diet: Mediterranean, rich in omega-3, vegetables, fruits, and whole grains.
  • Omega-3 fatty acids (2-4g/day EPA/DHA): 20-30% CRP reductions.
  • Increase fibre (25-40g/day): Particularly prebiotic fibres, 15-25% reductions.
  • Adequate sleep (7-9 hours): Sleep deprivation is strongly linked to inflammation.
  • Stress reduction: Meditation, yoga → 10-20% CRP reductions.
  • Statins (if indicated): Independent anti-inflammatory effect, 15-40% CRP reduction.
  • Curcumin (500-1000mg/day with piperine): 25-50% reductions in multiple trials.
  • Ginger (2-3g/day): Anti-inflammatory effects, 10-20% CRP reduction.
  • Green tea (3-5 cups/day): Polyphenols reduce inflammation.
  • Vitamin D sufficiency: Maintain >30 ng/mL, deficiency linked to elevated CRP.
  • Polyphenol-rich foods: Berries, dark chocolate, red wine (moderate), and olive oil.
  • Probiotic supplementation: May reduce CRP 10-20% via gut-immune axis.
  • Quit smoking: Can reduce CRP 20-30% within 6 months.

AVOID (Things That Increase CRP):

  • Obesity: Each 5-point BMI increase → 50% higher CRP.
  • Sedentary lifestyle: Independent inflammatory stimulus.
  • Smoking: 2-3x higher CRP levels in smokers.
  • Trans fats: Strongly pro-inflammatory.
  • High glycemic load diet: Refined carbs, sugars drive inflammation.
  • Excess omega-6 fatty acids: Particularly when omega-3 intake is low (high ratio problematic).
  • Processed meats: Nitrites, AGEs, and saturated fat combination is inflammatory.
  • Excess alcohol: >2 drinks/day increases inflammation.
  • Sleep deprivation: <6 hours → 40-50% higher CRP.
  • Chronic stress/depression: Psychological stress → inflammatory cytokines.
  • Poor oral hygiene: Periodontal disease significantly elevates CRP.
  • Certain medications: Hormone replacement therapy (oral estrogen) can increase CRP.
  • Uncontrolled chronic diseases: Diabetes, autoimmune conditions, sleep apnea.
  • Air pollution exposure: PM2.5 exposure is inflammatory.

 

White Blood Cell Count (WBC)

OPTIMISE (Maintain Optimal Range – Not Too High, Not Too Low):

  • Regular moderate exercise: 150 min/week maintains a healthy immune balance.
  • Anti-inflammatory diet: Mediterranean pattern supports optimal WBC levels.
  • Adequate sleep (7-9 hours): Critical for immune regulation.
  • Stress management: Chronic stress elevates cortisol → elevated WBC.
  • Maintain a healthy weight: Obesity is associated with chronic elevation.
  • Adequate micronutrients: Zinc, selenium, vitamin D, B vitamins for immune function.
  • Probiotic foods: Fermented foods support immune regulation via the gut.
  • Avoid over-exercise: Excessive training (>10 hours/week intense) can suppress immunity.
  • Omega-3 fatty acids: Help maintain anti-inflammatory balance.
  • Adequate protein: 1.6-2.2g/kg supports immune cell production without excess.

AVOID (Things That Dysregulate WBC):

  • Smoking: Chronically elevates WBC 20-30%, inflammatory state.
  • Obesity: Adipose tissue inflammation → chronic WBC elevation.
  • Chronic stress: Sustained cortisol → elevated WBC and impaired function.
  • Sleep deprivation: Disrupts circadian immune regulation.
  • Excessive alcohol: Impairs WBC function and production.
  • High sugar intake: Temporarily suppresses neutrophil function for hours.
  • Sedentary lifestyle: Associated with chronic low-grade inflammation.
  • Chronic infections: Undiagnosed dental, urinary, or other infections.
  • Air pollution: PM2.5 exposure elevates WBC.
  • Corticosteroid use/withdrawal: Can cause fluctuations.
  • Severe caloric restriction: Can suppress WBC production.

 

eGFR (Estimated Glomerular Filtration Rate)

OPTIMISE (Higher is Better, Prevent Decline):

  • Blood pressure control: Target <130/80, this is the most critical kidney-protective measure.
  • Glucose control: HbA1c <7% if diabetic, prevents diabetic nephropathy.
  • ACE inhibitors or ARBs: If hypertensive/diabetic, directly protect the kidneys.
  • Adequate hydration: 2-3L water/day prevents nephron stress.
  • DASH or Mediterranean diet: Reduces kidney disease progression risk.
  • Regular exercise: 150+ min/week maintains kidney function.
  • Maintain a healthy weight: Obesity increases glomerular hyperfiltration.
  • SGLT2 inhibitors (if diabetic): Empagliflozin and dapagliflozin slow kidney decline.
  • Limit sodium (<2300mg/day): Reduces BP and proteinuria.
  • Adequate but not excessive protein: 1.6-2.2g/kg for general health; if CKD, may need 0.6-1.2g/kg.
  • Omega-3 fatty acids: Anti-inflammatory, may slow decline.
  • Avoid nephrotoxic medications: NSAIDs, certain antibiotics, proton pump inhibitors (chronic use).
  • Treat underlying conditions: Diabetes, hypertension, autoimmune diseases.
  • Coenzyme Q10 (100-200mg/day): Some evidence for kidney protection.

AVOID (Things That Damage Kidneys/Reduce eGFR):

  • NSAIDs (chronic use): Ibuprofen, naproxen reduce kidney blood flow → lower eGFR.
  • Uncontrolled hypertension: The single greatest risk factor for kidney disease.
  • Uncontrolled diabetes: Diabetic nephropathy develops in 20-40% of diabetics.
  • High sodium intake: >3000mg/day accelerates decline.
  • Smoking: Direct nephrotoxicity, 40% faster kidney decline.
  • Excess protein: >2.0g/kg, chronically, may stress the kidneys in susceptible individuals.
  • Dehydration: Chronic under-hydration damages nephrons.
  • Obesity: Glomerular hyperfiltration and inflammation.
  • Nephrotoxic supplements: Some herbal products and aristolochic acid-containing herbs.
  • Proton pump inhibitors (chronic use): Associated with acute interstitial nephritis.
  • Contrast dye: If CKD present, risk of contrast-induced nephropathy.
  • Certain antibiotics: Aminoglycosides, vancomycin (need monitoring).
  • Excessive alcohol: Direct nephrotoxicity.
  • Illicit drugs: Cocaine, heroin, and MDMA cause kidney damage.
  • Calcineurin inhibitors: Tacrolimus, cyclosporine (if using for transplant/autoimmune).

 

TSH (Thyroid Stimulating Hormone)

OPTIMISE (Maintain Optimal Range – Not Too High, Not Too Low):

  • Adequate iodine (150-220mcg/day): Insufficient in some regions, but avoid excess.
  • Selenium (55-200mcg/day): Critical cofactor for thyroid hormone conversion.
  • Zinc (8-11mg/day): Required for TSH receptor function.
  • Iron sufficiency: Anaemia impairs thyroid hormone synthesis.
  • Vitamin D sufficiency: >30 ng/mL, deficiency linked to thyroid dysfunction.
  • Stress management: Chronic stress impairs HPT axis.
  • Adequate sleep: Sleep deprivation affects thyroid function.
  • Avoid excessive raw cruciferous: Goitrogens can interfere when consumed in large amounts raw (cooked is generally fine).
  • Tyrosine supplementation (if deficient): Precursor to thyroid hormones.
  • Ashwagandha (300-600mg/day): May normalise TSH in subclinical hypothyroidism.
  • Address autoimmunity: If Hashimoto’s, a gluten-free diet trial may help some individuals.
  • Regular exercise: Supports healthy HPT axis function.

AVOID (Things That Dysregulate TSH/Thyroid):

  • Iodine deficiency: The most common cause of hypothyroidism globally.
  • Iodine excess: >1000mcg/day can paradoxically suppress thyroid or trigger autoimmunity.
  • Soy isoflavones (excess): >100mg/day may interfere with thyroid function.
  • Goitrogenic foods in excess: Large amounts of raw cruciferous vegetables, and/or cassava.
  • Certain medications: Lithium, amiodarone, interferon-alpha, and tyrosine kinase inhibitors.
  • Chronic stress: HPA axis dysfunction → HPT axis dysregulation.
  • Selenium deficiency: Impairs T4 to T3 conversion.
  • Iron deficiency: Required for thyroid peroxidase function.
  • Fluoride excess: May interfere with iodine uptake (controversial).
  • Chronic inflammation: Autoimmune thyroiditis (Hashimoto’s, Graves’).
  • Excessive endurance exercise: Can suppress thyroid in some athletes.
  • Very low-calorie diets: <1000 kcal/day → metabolic slowdown, reduced T3.
  • Sleep apnea: Associated with thyroid dysfunction.
  • Gluten (if Hashimoto’s present): Molecular mimicry may worsen autoimmunity in susceptible.

 

Fitness Markers

VO₂ Max (Maximal Oxygen Uptake)

OPTIMISE (Higher is Better):

  • High-Intensity Interval Training (HIIT): 2-3x/week, 4×4 min protocol → 10-15% improvements in 8-12 weeks.
  • Zone 2 cardio: 3-4x/week, 45-60 min at ~70% max HR builds aerobic base → 8-12% gains.
  • Progressive overload: Gradually increase intensity, duration, frequency over months.
  • Cross-training: Mixing running, cycling, rowing, and swimming for balanced adaptation.
  • Altitude training: Natural or simulated, increases VO₂max 3-5%.
  • Weight loss (if overweight): Each 1kg lost → ~0.3-0.5 ml/kg/min improvement in relative VO₂max.
  • Beetroot juice/nitrates: 500-800mg nitrate pre-exercise may improve performance 1-3%.
  • Iron sufficiency: Critical for oxygen transport; anaemia drastically impairs VO₂max.
  • Adequate sleep: Recovery is essential for adaptations.
  • Periodisation: Structured training cycles optimise improvements.
  • Long slow distance: 2-3x/week builds capillary density, and mitochondrial density.
  • Strength training: Maintains muscle mass, improves neuromuscular economy.
  • Beta-alanine (3-6g/day): Buffers lactate, may improve performance 2-3%.

AVOID (Things That Reduce VO₂ Max):

  • Sedentary lifestyle: Single greatest factor in VO₂max decline (1% per year vs 0.5% with training).
  • Detraining: 2-4 weeks inactivity → 4-10% decline; 2-3 months → 15-20% decline.
  • Smoking: 10-15% lower VO₂max in smokers, impairs oxygen transport and utilisation.
  • Excess body fat: Each 1% body fat gain → ~0.2-0.3 ml/kg/min decline in relative VO₂max.
  • Anaemia: Iron, B12, folate deficiency severely impairs oxygen-carrying capacity.
  • Chronic overtraining: Without adequate recovery → plateaus, regression.
  • Poor sleep: <6 hours chronically impairs recovery and adaptations.
  • Alcohol excess: Impairs recovery, mitochondrial function.
  • Dehydration: Even 2% body weight loss from dehydration → 10-20% performance decline.
  • Chronic stress: Elevated cortisol impairs recovery and anabolic processes.
  • Ageing: ~1% per year decline after age 35 if untrained; ~0.5% if trained.
  • Air pollution exposure: Chronic exposure impairs respiratory and cardiovascular function.
  • Altitude illness: Without proper acclimatisation.

 

Resting Heart Rate (RHR)

OPTIMISE (Lower is Better, Up To A Point):

  • Regular aerobic exercise: 150-300 min/week → 5-15 bpm reduction over 3-6 months.
  • Improve cardiovascular fitness: Higher VO₂max correlates with lower RHR.
  • Weight loss (if overweight): 5-10% weight loss → 5-10 bpm reduction.
  • Adequate sleep (7-9 hours): Chronic sleep debt elevates RHR.
  • Stress management: Meditation, deep breathing → 5-8 bpm reductions.
  • Beta-blockers (if indicated medically): Can lower RHR 10-20 bpm.
  • Stay hydrated: Dehydration raises RHR.
  • Limit caffeine: If sensitive, reducing intake can lower RHR 5-10 bpm.
  • Quit smoking: 5-10 bpm reduction within weeks.
  • Magnesium (if deficient): Supports cardiac muscle relaxation.
  • Zone 2 training: Long, slow cardio builds parasympathetic tone.
  • Yoga/breathwork: Activates the parasympathetic nervous system.

AVOID (Things That Increase RHR):

  • Sedentary lifestyle: The deconditioned heart must work harder at rest.
  • Dehydration: Even mild dehydration → 3-5 bpm increase.
  • Sleep deprivation: Each hour of lost sleep → ~2 bpm increase.
  • Chronic stress/anxiety: Sustained sympathetic activation.
  • Excess caffeine: >400mg/day can elevate RHR 5-10 bpm.
  • Stimulants: Energy drinks, pre-workout supplements, decongestants.
  • Alcohol: Elevates RHR for 12-24 hours post-consumption.
  • Smoking: 5-10 bpm higher in smokers.
  • Obesity: Each 10kg excess → 2-3 bpm increase.
  • Overtraining: Elevated resting HR indicates inadequate recovery.
  • Fever/illness: Infection raises RHR ~10 bpm per degree Celsius.
  • Anaemia: The heart compensates for reduced oxygen-carrying capacity.
  • Hyperthyroidism: Elevated thyroid → higher resting HR.
  • Certain medications: Stimulants, decongestants, bronchodilators.
  • Poor thermoregulation: Excessive heat/cold exposure.

 

Heart Rate Variability (HRV – rMSSD)

OPTIMISE (Higher is Better):

  • Regular moderate exercise: 150 min/week → 10-20% HRV improvements (but avoid overtraining).
  • Stress management: Meditation, mindfulness → 20-40% improvements in 8-12 weeks.
  • Adequate sleep (7-9 hours): Single most important factor for HRV recovery.
  • Consistent sleep schedule: Regular bed/wake times optimise HRV.
  • Limit alcohol: Abstinence or ≤1 drink improves HRV.
  • Weight loss (if overweight): 5-10% weight loss → 10-20% HRV improvement.
  • Omega-3 fatty acids (2-4g/day): 10-15% HRV improvements via autonomic balance.
  • Yoga/breathwork: Slow breathing (5-6 breaths/min) → immediate HRV increases.
  • Cold exposure: Cold showers, ice baths may boost HRV via hormetic stress.
  • Magnesium (300-400mg/day): Supports parasympathetic function.
  • Quit smoking: Significant HRV improvements within weeks.
  • Moderate sauna use: 2-3x/week may improve HRV via autonomic conditioning.
  • Avoid late-night eating: Finish meals 3+ hours before bed for better HRV.
  • Low-intensity cardio: Zone 2 training builds vagal tone.
  • Ashwagandha (300-600mg/day): Adaptogen may improve HRV via stress reduction.

AVOID (Things That Reduce HRV):

  • Overtraining: Excessive training load without recovery → 20-40% HRV decline.
  • Sleep deprivation: <6 hours → significant HRV suppression.
  • Alcohol consumption: Even moderate intake reduces HRV for 24-48 hours.
  • Chronic stress: Sustained sympathetic dominance.
  • Irregular sleep schedule: Circadian disruption impairs HRV.
  • Late-night meals: Digestive stress during sleep reduces HRV.
  • Dehydration: Reduces HRV via increased sympathetic tone.
  • High-intensity training without recovery: Back-to-back hard days suppress HRV.
  • Smoking: Autonomic dysfunction, reduced HRV.
  • Excess caffeine: >400mg/day or late-day consumption.
  • Obesity: Particularly visceral fat, inflammatory cytokines reduce HRV.
  • Uncontrolled diabetes: Autonomic neuropathy reduces HRV.
  • Air pollution exposure: PM2.5 reduces HRV acutely.
  • Psychological stress: Anxiety and depression are strongly linked to low HRV.
  • Certain medications: Beta-agonists, stimulants, reduce HRV.

 

Body Composition

Body Fat Percentage

OPTIMISE (Achieve Optimal Range: Males 8-15%, Females 12-20%):

  • Caloric Appropriate Diet: For most people, this will mean a period of a calorie deficit, and then maintenance. 
  • Adequate protein intake (1.6-2.2g/kg): Preserves muscle during fat loss, increases satiety.
  • Resistance training: 3-4x/week prevents muscle loss during deficit and builds muscle which increases metabolism.
  • Adequate cardio: 150-300 min/week enhances fat oxidation.
  • Sleep optimisation (7-9 hours): Inadequate sleep → muscle loss over fat loss.
  • Increase NEAT: Non-exercise activity (walking, fidgeting) burns 300-800 kcal/day.
  • Progressive diet breaks: ~2 weeks maintenance every ~8-12 weeks prevents metabolic adaptation.
  • Green tea/caffeine: May enhance fat oxidation 3-5%.
  • Track consistently: Food logging increases adherence and success.

AVOID (Things That Increase Body Fat):

  • Chronic caloric surplus: Even 100 kcal/day excess → 5kg fat gain per year.
  • Avoid aggressive deficits: >750 kcal deficit → muscle loss, metabolic slowdown.
  • Sedentary lifestyle: <4000 steps/day strongly linked to fat gain.
  • Refined carbohydrates: Low satiety, promotes overconsumption.
  • Liquid calories: Soda, juice, and alcohol bypass satiety mechanisms.
  • Ultra-processed foods: Engineered for overconsumption, low satiety.
  • Sleep deprivation: <6 hours → increased hunger hormones, preferential muscle loss.
  • Chronic stress: Elevated cortisol → visceral fat accumulation.
  • Alcohol excess: 7 kcal/g with no satiety, inhibits fat oxidation for hours.
  • Late-night eating: Circadian misalignment may promote fat storage.
  • Excessive cardio without resistance training: Can lead to “skinny fat” phenotype.
  • Thyroid dysfunction: Uncontrolled hypothyroidism impairs fat metabolism.
  • Certain medications: Antipsychotics, some antidepressants, corticosteroids.
  • Menopause (unavoidable): Hormonal changes promote fat gain without intervention.

 

Waist Circumference

OPTIMISE (Lower is Better: Males <90cm, Females <80cm):

  • All strategies for reducing body fat (see Body Fat % section).
  • Visceral fat reduction: Prioritise cardio + resistance training combination.
  • Mediterranean diet: Specifically reduces visceral adiposity vs other diets.
  • HIIT training: Superior for visceral fat loss vs steady-state cardio.
  • Adequate sleep: <6 hours associated with 2-5cm greater waist.
  • Stress management: Cortisol drives visceral fat accumulation.
  • Limit alcohol: Particularly beer, associated with abdominal obesity.
  • Increase protein: High protein diets preferentially reduce abdominal fat.
  • Soluble fibre (10-25g/day): Specifically targets visceral fat.
  • Probiotics: May modestly reduce waist circumference via metabolic effects.
  • Avoid trans fats completely: Uniquely drives visceral fat accumulation.
  • Green tea (3-5 cups/day): Catechins may preferentially target abdominal fat.

AVOID (Things That Increase Waist Circumference):

  • Sedentary lifestyle: Sitting time directly correlated with waist size.
  • Trans fats: Drive visceral fat accumulation more than other fats.
  • Excess fructose/sugar: Particularly beverages, directly lipogenic to the liver and viscera.
  • Alcohol excess: “Beer belly” is real – alcohol → visceral fat.
  • Chronic stress: Cortisol → preferential visceral deposition.
  • Sleep deprivation: <6 hours → 2-3cm larger waist on average.
  • Smoking: Paradoxically increases visceral fat despite lower total weight.
  • High glycemic foods: Rapid insulin spikes promote abdominal fat storage.
  • Menopause (natural): Hormonal shift promotes visceral accumulation.
  • Cortisol excess: Cushing’s syndrome or chronic steroid use.
  • Low testosterone (males): Hypogonadism → visceral obesity.
  • Hypothyroidism: Slowed metabolism favours fat accumulation.

 

BMI (Body Mass Index)

OPTIMISE (Optimal Range: 20-25 kg/m²):

  • Balanced caloric intake: Match energy expenditure for maintenance.
  • If overweight (BMI >25): Apply fat loss strategies (see Body Fat % section).
  • If underweight (BMI <20): Caloric surplus + resistance training to build muscle.
  • Regular exercise: Maintain muscle mass while managing fat levels.
  • Mediterranean or DASH diet: Supports healthy weight maintenance.
  • Adequate protein: Prevents muscle loss, supports healthy composition.
  • Resistance training: Builds metabolically active tissue.
  • Monitor consistently: Weekly weigh-ins help maintain awareness.
  • Avoid yo-yo dieting: Stable weight is better than cycling.

AVOID (Things That Increase BMI Unhealthily):

  • Chronic caloric surplus: Primary driver of weight gain.
  • Ultra-processed foods: Engineered to promote overconsumption.
  • Sedentary lifestyle: NEAT reduction major contributor.
  • Liquid calories: Beverages don’t trigger satiety.
  • Sleep deprivation: Hormonal changes promote weight gain.
  • Stress eating: Cortisol + emotional eating behaviour.
  • Medications: Antipsychotics, some antidepressants, corticosteroids.
  • All factors listed in Body Fat % section

 

Fat-Free Mass Index (FFMI)

OPTIMISE (Optimal Range: Males 22-25, Females 15-22 kg/m²):

  • Progressive resistance training: 3-5x/week with compound movements.
  • Protein intake (1.6-2.2g/kg): Essential for muscle protein synthesis.
  • Caloric surplus (if building): +300-500 kcal/day for lean gains.
  • Adequate carbohydrates: 3-5g/kg for training fuel and recovery.
  • Creatine monohydrate (5g/day): ~1-2kg lean mass gain is typical.
  • Adequate sleep (7-9 hours): Growth hormone, testosterone release during sleep.
  • Progressive overload: Gradually increase weight, volume, intensity.
  • Leucine-rich proteins: Whey, chicken, beef optimise muscle protein synthesis.
  • Testosterone optimisation: Maintain healthy levels (see Testosterone section).
  • Beta-alanine (3-6g/day): Buffers lactate, allows more training volume.
  • Avoid excessive cardio: >300 min/week interferes with hypertrophy.

AVOID (Things That Reduce FFMI/Muscle Mass):

  • Inadequate protein: <1.2g/kg → muscle loss during deficit or ageing.
  • Excessive cardio: The interference effect reduces strength/hypertrophy gains (can be somewhat offset by simply eating enough).
  • Caloric deficit without resistance training: Muscle lost along with fat.
  • Sleep deprivation: <6 hours → 60% of weight loss from muscle vs fat.
  • Alcohol excess: Impairs muscle protein synthesis for 24+ hours.
  • Sedentary lifestyle: Use it or lose it – sarcopenia begins by age 30.
  • Ageing (natural): 3-8% muscle loss per decade after age 30 if untrained.
  • Glucocorticoids: Catabolic, muscle wasting effect.
  • Inadequate total calories: Even with protein, severe restriction → muscle loss.
  • Overtraining: Without recovery, breaks down more than builds.
  • Testosterone deficiency: Critical for muscle protein synthesis.
  • Chronic inflammation: IL-6, TNF-alpha catabolic to muscle.
  • Immobilisation: Bed rest, injury → rapid muscle atrophy.
  • Certain medications: Statins (rarely), corticosteroids, chemotherapy.

 

Waist-to-Height Ratio (WHtR)

OPTIMISE (Lower is Better: <0.50):

  • All strategies for reducing waist circumference (see Waist section)
  • Note: Height is fixed, so this is entirely about waist reduction

AVOID (Things That Increase WHtR):

  • Same as Waist Circumference section – all factors that increase visceral fat

 

Strength Markers

Squat 1RM (×Bodyweight)

OPTIMISE (Higher is Better: Males >2.0×BW, Females >1.5×BW):

  • Progressive squat training: 1-3x/week with progressive overload.
  • Periodisation: Linear or undulating programs can help to optimise strength gains.
  • Compound focused leg training: Back squats, front squats, Bulgarian splits, lunges etc.
  • Adequate volume: 10-20 sets per week for the muscles involved.
  • Protein intake (1.6-2.2g/kg): Supports strength and recovery.
  • Creatine monohydrate (5g/day): 5-10% strength gains are fairly typical (less the stronger you are, and less if you already eat meat).
  • Adequate carbs: 3-5g/kg fuels high-intensity training.
  • Technique focus: Video analysis and direct coaching generally improves strength.
  • Mobility work: Hip, ankle, and thoracic mobility allows deeper squats.
  • Core strengthening: Planks, dead bugs, Pallof press improve brace strength.
  • Sleep optimisation (7-9 hours): Neural recovery is critical for strength.
  • Explosive training: Box jumps and jump squats build rate of force development.
  • Address weak points: If glutes are weak, prioritise hip thrusts; if quads weak, front squats/hack squats/leg presses.

AVOID (Things That Reduce Squat Strength):

  • Inadequate training frequency: <1x/week insufficient for adaptation, unless you are already very strong.
  • Poor technique: Reduces force production, increases injury risk.
  • Inadequate recovery: Training the same muscle groups on consecutive days.
  • Excessive cardio: >300 min/week cardio can reduce strength gains (interference effect).
  • Caloric deficit without high protein: Lose muscle and strength during cuts.
  • Sleep deprivation: <6 hours → 10-20% strength reduction.
  • Alcohol excess: Impairs recovery, reduces protein synthesis.
  • Inadequate mobility: Hip/ankle restrictions limit depth and power.
  • Overtraining without auto-regulation/deloads: CNS fatigue, strength plateau/regression.
  • Injuries: Train around, not through pain.
  • Ageing (natural): 1-2% strength loss per year after age 40 if untrained.

 

Deadlift 1RM (×Bodyweight)

OPTIMISE (Higher is Better: Males >2.5×BW, Females >2.0×BW):

  • Progressive deadlift training: 1-2x/week (recovery-demanding).
  • Variation: Conventional, sumo, Romanian, trap bar for balanced development.
  • Posterior chain focus: Hamstrings, glutes, erectors are primary movers.
  • Hip hinge pattern mastery: Kettlebell swings, Romanian DLs for technique.
  • Grip strength training: Farmer’s carries, dead hangs, fat gripz, direct grip training.
  • Back strengthening: Rows, pull-ups support spinal stability.
  • Progressive overload: Gradual weight increases over months.
  • Technique refinement: Bar path, hip positioning, bracing critical.
  • Adequate protein (1.6-2.2g/kg): Essential for recovery.
  • Creatine monohydrate (5g/day): 5-10% strength gains are fairly typical (less the stronger you are, and less if you already eat meat).
  • Lifting straps: Allow overload beyond grip limitations.
  • Deficit deadlifts: Builds strength from a difficult position.
  • Block pulls: Overload the top portion of the lift.
  • Adequate rest: 2-5 min between heavy sets

AVOID (Things That Reduce Deadlift Strength):

  • Poor form: Rounded back, improper bracing → injury and reduced power.
  • Overtraining: Deadlifts are CNS-intensive; >2x/week often counterproductive.
  • Inadequate grip strength: Limits load, use straps strategically.
  • Weak posterior chain: Neglecting hamstrings, glutes limits deadlift.
  • Poor hip mobility: Restricts hip hinge depth and power.
  • Inadequate core strength: Limits brace strength, reduces force transfer.
  • Excessive volume: Deadlifts require longer recovery than other lifts.
  • All factors from the Squat section apply: Sleep, nutrition, recovery.

 

Bench Press 1RM (×Bodyweight)

OPTIMISE (Higher is Better: Males >1.5×BW, Females >1.0×BW):

  • Progressive bench training: 2-3x/week with varied intensity.
  • Volume work: Flat, incline, dumbbell variations for complete development.
  • Accessory work: Triceps extensions, shoulder presses, rows for support.
  • Technique optimisation: Leg drive, arch, and retracted scapulae all increase leverage.
  • Progressive overload: Add weight, reps, or sets over time.
  • Adequate volume: 10-20 sets per week for the muscles involved.
  • Strong foundation: Develop back (rows), shoulders, triceps.
  • Protein intake (1.6-2.2g/kg): Supports hypertrophy.
  • Creatine supplementation: 5+g/day for strength gains.
  • Address weak points: If triceps are weak, add more direct isolation work; if chest is weak, add more direct isolation work.
  • Pause reps: Build strength from a dead stop.
  • Board presses/pin presses: Overload lockout portion.
  • Shoulder health: Face pulls, band pull-aparts, and external rotations potentially help prevent shoulder issues.

AVOID (Things That Reduce Bench Strength):

  • Shoulder injuries: Impingement, rotator cuff issues are very common.
  • Poor technique: Flared elbows, no leg drive, inconsistent bar path.
  • Inadequate back development: Weak upper back limits bench stability.
  • Overtraining chest: >20 sets/week is often counterproductive.
  • Neglecting triceps: Lockout strength critical for heavy weights.
  • Poor shoulder mobility: Internal rotation deficits are common in benchers.
  • Inadequate rest: Ideally you want 2-5 min between heavy sets at a minimum.
  • All general strength factors: Sleep, nutrition, recovery.

 

Chin-ups (Strict Reps)

OPTIMISE (Higher is Better: Males >15 reps, Females >12 reps):

  • Progressive training: Greasing the groove (frequent submaximal sets throughout the day).
  • Weighted chin-ups: Low rep, heavy weight builds max strength.
  • Eccentric training: Slow negatives (5-10 sec) build strength.
  • Assistance work: Rows and lat pulldowns support pulling strength.
  • Grip strength: Dead hangs, farmer’s carries, and direct grip work improve endurance.
  • Frequency: 2-5x/week, varied intensity and volume.
  • Reduce body fat: Each 1% body fat loss → ~1 additional rep capability.
  • Progressive overload: Add weight, reps, volume or frequency.
  • Address weak points: If biceps are weak, add curls; if lats are weak, add lat pull downs or rows.
  • Full range of motion: Dead hang to chin over bar.
  • Adequate protein: Supports muscle recovery and growth.
  • Grip variations: Supinated, pronated, neutral for balanced development.
  • Banded assistance: Build strength while maintaining good form.

AVOID (Things That Reduce Chin-up Performance):

  • Excess body weight: Extra 5kg bodyweight → 3-5 fewer reps typically.
  • Poor technique: Kipping, partial ROM inflates numbers but reduces strength.
  • Inadequate back training: Rows and vertical pulls are essential.
  • Grip weakness: Limits endurance even if back/biceps are strong.
  • Overtraining: Daily max effort sets lead to overuse injuries.
  • Elbow/shoulder injuries: Golfer’s elbow, and impingement are common.
  • Inadequate recovery: Pulling muscles need 48+ hours between hard sessions.
  • All general strength factors: Sleep, nutrition, recovery.

 

Recovery & Sleep

Sleep Quantity

OPTIMISE (Target: 7-9 Hours per Night):

  • Consistent sleep schedule: Same bed/wake time every day, even weekends.
  • Sleep hygiene: Dark, cool (16-19°C), quiet bedroom.
  • Limit blue light exposure: No screens 1-2 hours before bed or use blue blockers.
  • Morning sunlight: Bright light within 30 minutes of waking sets the circadian rhythm.
  • Avoid caffeine after noon: Half-life 5-6 hours, affects sleep architecture.
  • Limit alcohol: Disrupts REM sleep, even if it helps falling asleep.
  • Regular exercise: 150+ min/week improves sleep quality and duration.
  • Magnesium glycinate (300-400mg before bed): Promotes relaxation.
  • Avoid large meals 2-3 hours before bed: Digestive stress impairs sleep.
  • Stress management: Meditation and journaling reduce rumination.
  • White noise/earplugs: Blocks disruptive sounds.
  • Melatonin (0.3-5mg): If circadian rhythm disruption or jet lag.
  • L-theanine (200-400mg): Promotes relaxation without sedation.
  • Glycine (3g before bed): Improves sleep quality in some individuals.
  • CBD (10-25mg): May improve sleep in anxiety-related insomnia.
  • Address sleep apnea: If snoring, witnessed apneas, morning headaches.

AVOID (Things That Reduce Sleep Quantity/Quality):

  • Irregular sleep schedule: Shifts bedtime by >1 hour impairs circadian rhythm.
  • Caffeine after 2 PM: Even if you “can sleep,” it reduces sleep quality.
  • Alcohol before bed: Fragments sleep, suppresses REM.
  • Large meals before bed: Digestive stress and acid reflux.
  • Bright lights evening: Suppresses melatonin, delays sleep onset.
  • Screen time in bed: Blue light and mental stimulation.
  • Exercise within 2-3 hours of bed: Can elevate core temp and arousal.
  • Stress/anxiety: Racing thoughts prevent sleep onset.
  • Bedroom too warm: >20°C impairs sleep onset and quality.
  • Napping after 3 PM: Can reduce nighttime sleep drive.
  • Sleeping pills long-term: Benzodiazepines reduce deep sleep, and tolerance develops.
  • Smoking: Nicotine is a stimulant, and you get withdrawal during the night, which disrupts sleep.
  • Shift work: Circadian disruption is very difficult to overcome.
  • Sleep apnea: Fragmented sleep, often undiagnosed.

 

Hormones

Testosterone (Males Only)

OPTIMISE (Higher is Better, Optimal: 21-42 nmol/L / 605-1211 ng/dL):

  • Adequate sleep (7-9 hours): Each hour of sleep <5 → ~15% testosterone reduction.
  • Maintain healthy weight: Obesity decreases T; 5-10% weight loss → 100-200 ng/dL increase.
  • Adequate dietary fat (20-35% calories): Ideally, fairly evenly spread across the day.
  • Zinc (15-30mg/day): Critical cofactor; deficiency drastically reduces testosterone.
  • Vitamin D (maintain >30 ng/mL): Supplementation may increase T 20-25% if deficient.
  • Magnesium (300-400mg/day): Reduces SHBG, increases free testosterone.
  • Reduce chronic stress: Cortisol antagonises testosterone production.
  • Limit alcohol (<2 drinks/day): Excess suppresses Leydig cells.
  • Boron (6-10mg/day): May increase free T by reducing SHBG.
  • Ashwagandha (600mg/day): 15-17% T increase in some studies.
  • Tongkat Ali (200-400mg): Some evidence for 15-35% increases.
  • TRT (if clinically indicated): Testosterone replacement for diagnosed hypogonadism.

AVOID (Things That Decrease Testosterone):

  • Obesity: Each 10-point BMI increase → ~100 ng/dL reduction.
  • Sleep deprivation: <5 hours → 10-15% testosterone reduction.
  • Chronic stress: Elevated cortisol suppresses GnRH → LH → testosterone.
  • Excess alcohol: >2 drinks/day chronically suppresses testicular function.
  • Opioid pain medications: Dramatic suppression, often <200 ng/dL.
  • Anabolic steroids: Exogenous androgens → testicular atrophy, suppressed natural production.
  • Certain medications: Statins (very modest), spironolactone, ketoconazole, some antipsychotics.
  • Marijuana/cannabis: THC suppresses testosterone dose-dependently.
  • Very low-fat diets: <15% calories from fat → 10-15% T reduction.
  • Endocrine disruptors: BPA, phthalates, pesticides (cumulative environmental effect).
  • Excessive endurance exercise: >10 hours/week without adequate recovery and/or calories.
  • Liquorice: Glycyrrhizin reduces testosterone.
  • Mint: Spearmint, peppermint may reduce T (more relevant in women).
  • Soy isoflavones: >100mg/day may suppress T in some men.
  • Ageing (natural): ~1-2% per year decline after age 30.
  • Varicocele: Testicular vein dilation, treatable surgically.
  • Hemochromatosis: Iron overload damages the testes.
  • Type 2 diabetes: Insulin resistance linked to 20-30% lower testosterone.

 

A Few Notes

Now, before you dive into implementing these strategies, I need you to understand some fundamental principles that apply across all of these metrics. 

 

1. Lifestyle First, Supplements Second, Medications Third

The most powerful interventions for across the board effects are diet, exercise, sleep, and stress management.  Supplements offer modest benefits, we’re talking 5-15% improvements in some cases, for specific issues. They’re the icing on the cake, not the cake itself. 

And medications are for when lifestyle changes are insufficient or when you need rapid risk reduction because your numbers are dangerously high. Some medications are orders of magnitude more effective than lifestyle interventions, but they generally don’t provide the full spectrum of benefits that lifestyle changes do, and you are almost always supposed to make the lifestyle changes along with medication. 

I see people all the time who want to pop a supplement or get a prescription without changing their diet or starting to exercise, but that’s backwards. A statin might drop your LDL by 40%, but if you’re still eating junk, sitting all day, and sleeping 5 hours a night, you’re fighting a losing battle, because this is still negatively affecting all your other markers. Yes, you have fixed the immediate danger, but you have not fixed the foundation yet.

 

2. Consistency Beats Intensity 

Moderate efforts sustained for years will generally beat heroic efforts abandoned after weeks. The person who exercises 3x/week for 30 years will have dramatically better health outcomes than the person who goes hard 6x/week for 3 months, burns out, and quits. The person who makes sustainable dietary improvements they can maintain indefinitely will beat the person who does a strict elimination diet for 8 weeks, then rebounds.

This is a marathon, not a sprint. Actually, it’s not even a marathon, it’s just your life. You need to build habits you can sustain for decades, not pursue perfection for weeks. The compound effect only works if you’re consistent over time.

 

3. The Stoic Dichotomy: Control What You Can, Accept What You Cannot

The ancient Stoic philosopher Epictetus taught what he called the “dichotomy of control”. This is the fundamental division between what’s within your control and what’s not. He argued that the key to peace of mind is focusing maximum effort on what you can control while accepting what you cannot.

This applies directly to these health trajectories:

 

What You Cannot Control:

  • Your genetic predispositions (cardiovascular disease runs in your family, tendency to gain weight easily).
  • The passage of time (you will age).
  • True biological ageing (some metrics will decline even with optimisation).
  • Random health events (accidents, random cancers, genetic diseases).
  • The obesogenic environment you live in (ultra-processed foods everywhere, sedentary jobs).

What You Can Control:

  • Your training frequency, intensity, and consistency.
  • Your food choices and portions.
  • Your sleep schedule and sleep hygiene.
  • Your stress management practices.
  • Whether you smoke or drink excessively.
  • Who you spend time with (social environment).
  • How you respond to setbacks.

The optimisation trajectory is Stoicism applied to health: maximum effort on what’s within your control, acceptance of what’s not.

You cannot prevent your VO₂ max from declining somewhat with age, that’s biology. But you can control whether it declines 53% (natural) or 16% (optimisation).

You cannot control your genetic predisposition to high cholesterol. But you can control whether you compound that predisposition with poor diet and inactivity, or whether you mitigate it through lifestyle optimisation and pharmaceuticals.

The trajectories on these charts are not outside events. They’re the mathematical accumulation of choices within your control. Every workout, every meal, and every night of sleep are largely inside your control.

Complaining about genetics, ageing, or “not having time” is what Epictetus would call focusing on externals; things outside your control. Wasted energy. Useless suffering. It is also what Jean-Paul Sartre would call “bad faith”, because you are trading away your autonomy and agency, rather than radically accepting that you are the maker of your own destiny. 

Focus on internals: Did you train today? Did you eat well? Did you do the things that would allow you to sleep adequately? Those are yours. Those determine your trajectory.

 

4. You Are Not a Population Average

Everything I’ve listed here represents population averages from research studies. But you are an individual with your own unique genetics, medical conditions, medications, and life circumstances.

Some people are hyper-responders to dietary cholesterol. Others can eat eggs every day, and their LDL barely moves. Some people are salt-sensitive and see massive blood pressure improvements from sodium restriction. Others? Not so much. Some people respond incredibly well to training. Others have genetic factors that make certain adaptations harder.

This is why you need to work with qualified healthcare providers who know your individual situation. Use these recommendations as a starting point, but track your own responses and adjust accordingly. What works for the average person might not be optimal for you.

 

5. Everything Is Connected

Improving one metric often improves many others simultaneously. Lose 10kg of fat and watch what happens: your blood pressure drops, your glucose and HbA1c improve, your lipid profile gets better, your inflammation markers decrease, your testosterone increases (if you’re a man), your liver enzymes improve, you sleep better, and your VO₂ max improves. One intervention, multiple benefits.

Start resistance training consistently: you build muscle, increase metabolic rate, improve insulin sensitivity, strengthen bones, boost testosterone, improve sleep quality, and reduce inflammation. Again, one intervention, systemic improvements.

This is why the optimisation trajectory works so well; you’re not just fixing isolated problems, you’re improving an integrated system. The interventions synergise with each other.

 

6. There Is No Magic Bullet

If someone is selling you a supplement or intervention that promises to dramatically improve a single metric without addressing the fundamentals, run away. “Take this supplement and drop your cholesterol 50% without changing your diet!” Nope. “Do this one weird trick to fix your blood pressure!” Doesn’t exist. “Reverse diabetes with this miracle berry extract!” Not happening.

Health is multifactorial. The interventions that work are often boring and unsexy: eat whole foods, exercise regularly, sleep 8 hours, manage stress, don’t smoke, limit alcohol. There’s no shortcut, no hack, and no secret that successful people know that you don’t.

The closest thing to a “magic bullet” is consistent execution of the boring fundamentals over decades. That’s the secret.

 

7. You Can’t Manage What You Don’t Measure

Regular testing allows you to see what’s working and what isn’t. For most people, annual to bi-annual comprehensive blood work is sufficient to track trends. However, if you’re actively optimising and making aggressive changes, quarterly testing makes sense so you can see the response to your interventions and make adjustments.

Don’t just test once, implement a bunch of changes, and assume it worked. Test, intervene, retest, adjust. That’s how you dial things in over time. And when you see that number improving keep a note of what has been working and what hasn’t. 

 

8. Lifestyle Complements Medicine, It Doesn’t Replace It

If your numbers are severely abnormal, you may need medical intervention, not just lifestyle changes. If your LDL is 6.0 mmol/L, you’re at very high cardiovascular risk, and you probably need a statin right now while you work on lifestyle. If your blood pressure is 180/110, you need medication immediately, not “let’s try beetroot juice for 3 months.” If your fasting glucose is 15 mmol/L, you need medical management of your diabetes, not just “cut out sugar and see what happens.”

Lifestyle optimisation is incredibly powerful, but it has limits. Work with your doctor. Take medications when indicated. Use lifestyle changes to reduce the dose you need or potentially come off medications eventually, but don’t refuse necessary medical care because you want to “do it naturally.”

 

9. The Older You Get, The More This Matters

As you saw in the trajectory charts, the rate of decline accelerates with age. The natural trajectory shows modest declines in your 30s and 40s, but by your 60s and 70s, the decline becomes much steeper.

This means interventions become more critical as you age. The 65-year-old needs to be more diligent about training, nutrition, and sleep than the 25-year-old if they want to maintain function. The margin for error gets smaller. 

But the good news is that the interventions still largely work at any age. You can start optimising at 60 and still make dramatic improvements. It’s just harder to achieve large gains, and maintenance becomes more critical.

 

10. Small Changes Compound Over Decades

Don’t overwhelm yourself trying to implement everything perfectly right now. Start where you are, make one or two changes you can sustain, master those, and then add more.

Can’t train 5x/week right now? Start with 2x/week consistently. Can’t overhaul your entire diet? Start by adding a serving of vegetables to each meal. Can’t sleep 8 hours yet? Work on getting 7 consistently first.

Small changes, sustained over years and decades, compound into massive results. The gap between natural decline and optimisation grows exponentially over time because of compounding. Every small positive change is a course correction that compounds over the years ahead.

Perfect is the enemy of good. Don’t let the pursuit of the optimal prevent you from doing the achievable.

 

The Seven Deadly Sins of Health Optimisation

You now know what to do. You understand the trajectories, the interventions, and even bits about the psychology of behaviour change. But knowing what to do and actually doing it successfully are different problems.

Over the years, I’ve watched hundreds of people sabotage themselves through specific, predictable patterns of self-defeating behaviour. These are the seven most common traps. If you recognise yourself in any of these, you’re not alone. But you do need to course-correct.

 

1. Paralysis by Analysis

The trap: Spending months “researching the perfect program” while taking zero action. Reading 47 books on nutrition. Watching 200 hours of fitness YouTube. Debating whether Starting Strength or StrongLifts 5×5 is superior. Agonising over whether to do IF 16:8 or 18:6. Never actually starting because you haven’t figured out the optimal approach yet.

Why it’s deadly: The difference between a good program executed consistently and a perfect program executed inconsistently is massive. The difference between a good program and a perfect program, both executed consistently, is trivial. You’re optimising 2% while ignoring the 98%.

The antidote: Pick any reasonable program from a credible source and execute it consistently for 12 weeks without changing anything. You’ll learn more from 12 weeks of consistent execution than from 12 months of research. Action produces information. Research produces procrastination disguised as productivity.

 

2. All-or-Nothing Thinking

The trap: “I missed Monday’s workout, so the week is ruined.” “I ate cake at the birthday party, so I might as well order pizza tonight.” “I can’t do my full 60-minute workout, so I won’t train at all.” One deviation from the plan becomes permission to abandon the plan entirely.

Why it’s deadly: Optimisation isn’t about perfection, it’s about consistency over time. A few missed workouts or imperfect meals scattered across months barely register. But the all-or-nothing spiral where one deviation becomes a week or month of abandonment? That destroys trajectories.

The antidote: Adopt the “Never Zero” principle religiously. Can’t do 60 minutes? Do 20. Can’t eat perfectly? Hit your protein target even if other things slip. Can’t get 8 hours of sleep? Get 7. Perfection isn’t the goal. Avoiding zero is the goal. A 60% effort sustained beats a 100% effort abandoned.

 

3. Metric Obsession

The trap: Checking blood pressure 5 times per day and panicking over normal fluctuations. Weighing yourself every morning and freaking out over water retention. Testing blood glucose after every meal. Tracking HRV obsessively and altering training based on single-day readings. You’ve turned optimisation into an anxiety disorder.

Why it’s deadly: Over-monitoring increases stress, which impairs the very metrics you’re trying to optimise. High-frequency measurement without understanding normal variability leads to random changes in protocol based on noise, not signal. You’re constantly “putting out fires” that are just normal biological variation.

The antidote: Establish a measurement schedule and stick to it. Weight: weekly (same day, same time). Blood work: quarterly if actively optimising, annually for maintenance. Blood pressure: weekly unless diagnosed with hypertension. HRV: look at 7-day rolling average, not daily. Treat metrics as tools for long-term trend analysis, not daily report cards.

 

4. Supplement Dependency

The trap: Spending €500/month on supplements while eating McDonald’s three times a week. Believing that the perfect stack of nootropics, adaptogens, and performance enhancers will compensate for 5 hours of sleep and zero strength training. Prioritising pills over proteins, powders over push-ups.

Why it’s deadly: Supplements offer very small percentage improvements on a solid foundation. On a broken foundation, they offer approximately zero. You’re spending huge amounts of money and mental energy on the least impactful interventions while ignoring the most impactful ones. It’s motivated reasoning; supplements feel like action without requiring actual behaviour change.

The antidote: Master the fundamentals first: train 4x/week consistently, hit protein targets, sleep 8 hours, manage stress. Do this for 6 months. Then, and only then, add supplements strategically to address specific deficiencies or optimisation goals. If you’re not doing the basics, the supplements are just expensive urine.

 

5. Outsourcing Responsibility

The trap: “My trainer will fix me.” “My nutritionist will tell me what to eat.” “My doctor will manage my health.” You’ve hired experts but abdicated all personal responsibility. You do what they say on Monday, but by Wednesday, you’re back to old habits. You’re waiting for someone else to care about your health more than you do.

Why it’s deadly: No one, no matter how qualified or well-intentioned, can want your health more than you do. Coaches, trainers, nutritionists, and doctors are tools to enhance your own efforts, not substitutes for your own efforts. External accountability helps, but if the motivation is purely external, it evaporates the moment supervision ends.

The antidote: Understand that experts are guides, not saviours. They can show you the path, but you have to walk it. Take radical responsibility: your health outcomes are your responsibility, regardless of how good your support team is. Learn the principles so you can self-correct when circumstances change. The goal is to internalise the process, not remain dependent on external control.

 

6. Social Isolation

The trap: You’ve discovered optimisation and become insufferable. You lecture friends about their diet. You refuse to attend any social event that might involve alcohol or non-optimal food. You’ve cut off everyone who isn’t on the same path. You’ve made health your entire identity and lost everything else. Your social media is exclusively gym posts and meal prep photos.

Why it’s deadly: Humans are social creatures. Relationships and social connections are themselves health-promoting. Chronic isolation and social conflict create psychological stress that negates many benefits of physical optimisation. You’re optimising yourself into loneliness, and loneliness is a stronger predictor of mortality than obesity.

The antidote: Optimisation should enhance your life, not replace it. Learn to navigate social situations flexibly. You can eat optimally 90% of the time and enjoy celebrations without guilt. You can train hard and also have friends who don’t train. You can be serious about health without being insufferable about it. The goal is to be the healthiest version of yourself while remaining a complete human being.

 

7. Moving the Goalposts

The trap: You achieve optimisation, and your metrics are in the optimal ranges, you feel great, you look great, you’re performing well. But instead of maintaining and enjoying it, you immediately find new problems. You need to get leaner. You need to get stronger. You need to optimise sleep even further. The target keeps moving. You’re never satisfied. Optimisation has become an obsession.

Why it’s deadly: There’s always another level. But at some point, the marginal returns become so small that the effort required creates more stress than benefit. You’ve crossed from optimisation into orthorexia or body dysmorphia. Your mental health is suffering in pursuit of physical health. 

The antidote: Define your “good enough” criteria in advance. What metrics in what ranges constitute success? When you hit those targets, maintain them for 6-12 months without changing anything. Enjoy the results. Let optimisation become your new normal rather than constantly reaching for the next level. Remember that the goal is living well, not perpetual self-improvement.

 

Each of these traps is seductive because it feels productive or virtuous. But they’re all forms of self-sabotage. If you recognise yourself in any of them, course-correct now. You are not trying to be perfect. This stuff doesn’t need to be all-consuming, you just need to be consistent.

 

Final Notes on Optimisation

Optimisation isn’t about being perfect. It’s not about doing everything on these lists. It’s about understanding the principles, implementing the interventions that are most relevant to your situation, being consistent over time, tracking your progress, and adjusting based on results.

The trajectories I’ve shown you aren’t destiny, they’re projections based on different behaviour patterns. You get to choose which pattern you follow. Every day, with every meal, every workout you do or skip, every night of good or poor sleep, you’re voting for which trajectory you’re on.

Now you know what the paths look like and what’s required to follow each one. The first question is; what are you going to do with this information? But the deeper question you must tackle is; what are you optimising for?

We’ve spent this entire article discussing health metrics, trajectories, and optimisation strategies. But there’s a deeper question we haven’t fully addressed: why does this matter? Not the surface answer of “to live longer” or “to be healthy.” The deeper answer. What are you actually optimising for?

Aristotle wrote about eudaimonia, which is often translated as “happiness” but more accurately meaning “human flourishing” or “living well.” It’s not about momentary pleasure or even about longevity per se. It’s about actualising your potential as a human being across a complete life. The natural decline trajectory is a slow abandonment of your physical potential. It’s choosing to become less capable, less vital, and less able to pursue what you value, year after year after year.

The optimisation trajectory is arete; the ancient Greek concept of excellence, virtue, and reaching your highest potential. It’s not about being perfect. It’s about being as good as you can be at the thing of being human. So, you don’t optimise for health. You optimise for what health enables. Health isn’t the goal. Health is the platform upon which everything else rests.

Agency (the capacity to make choices and act on them) requires health. When your VO₂ max drops to 21 ml/kg/min, you’ve lost the agency to hike, travel freely, play actively, and pursue physical hobbies. Your choices are constrained by your cardiovascular system.

Independence (self-sufficiency, not being a burden) requires strength and fitness. When you’ve lost 80% of your strength, you can’t get off the toilet unassisted, can’t carry your shopping, and can’t lift your children/grandchildren. You’ve lost independence.

Presence (being fully engaged with life instead of managing disease) requires metabolic health. When you’re on six medications, seeing specialists quarterly, dealing with complications of diabetes or heart disease, you’re no longer present in your life. Your life is managed by your diseases.

Dignity (living on your own terms until the end) requires all of the above.

The optimisation trajectory isn’t about adding years to your life, though it probably does that. It’s about adding life to your years. It’s about maintaining the physical capacity to remain the protagonist of your own story instead of becoming a side character limited by your declining body.

Existentialist philosopher Albert Camus wrote: “The literal meaning of life is whatever you’re doing that prevents you from killing yourself.” This is extremely dark, but the point is that meaning comes from engagement, from doing, from participating in life actively rather than observing it passively.

The natural trajectory slowly transforms you from participant to observer. You watch others hike while you sit in the car. You watch others play with grandchildren while you watch from a chair. You watch life happen around you, constrained by your body’s limitations.

The optimisation trajectory lets you stay a participant. Not forever, because nothing does and you must accept decline at some stage. But it does allow you to be an active participant in life for decades longer. And when the end comes, it comes quickly rather than slowly, and with dignity rather than slow, gruelling deterioration.

You’re not optimising for health. You’re optimising for agency, independence, presence, and dignity. Health is just the tool that makes those possible.

So the question isn’t really “should I follow the optimisation trajectory?” The question is: “what kind of person do I want to be, and what kind of life do I want to live, in my 60s, 70s, and 80s?”

Do you want to be the 75-year-old hiking mountains, or the 75-year-old struggling with stairs? The person who’s still travelling, or the person who can’t walk through an airport? The person who’s independent, or the person who needs assistance with basic activities? The person who’s present and engaged, or the person who’s managed by medications and diseases?

That’s the actual choice these trajectories represent. 

 

Triage Health Trajectory Tool Conclusion

Alright, we’ve covered a lot of ground here. You’ve seen the data. You understand the compound effect. You know what optimisation requires. You’ve got the numbers showing exactly where different behaviour patterns lead over 50 years. But before I give you the typical conclusion and the motivational call-to-action, the “so what are you going to do about it?”, I want to acknowledge something that most health and fitness content ignores:

You’re probably not going to do most of what this article recommends.

This is generally not because you’re lazy or weak-willed. It’s definitely not because you don’t care. Rather, it’s because behaviour change is genuinely hard, and most people who read this article will close the browser tab, intend to make changes, and then… life happens. Inertia wins. The red line continues.

I’ve been doing this long enough to know that reality. And I think you deserve honesty about it. So let me offer something different than the typical “you can do it!” motivational conclusion. Let me offer you a framework from psychology for actually making this work:

Existentialist philosopher Jean-Paul Sartre wrote that we are “condemned to be free”, and that we cannot escape the responsibility of choosing. Every day you don’t train is a choice. Every meal is a choice. Every night you don’t do your sleep hygiene habits is a choice.

Pretending you’re “too busy” or “too tired” or “will start next Monday” is what Sartre called “bad faith”. You’re denying your own agency, pretending you don’t have a choice when you absolutely do.

These trajectories make that undeniable: you are choosing your future health, whether you acknowledge it or not. The question is only whether you’re choosing consciously or unconsciously.

Here’s a psychological reframe that might hit harder: You’re not deciding whether to “gain” health. You’re deciding whether to keep what you already have. Right now, at whatever age you’re reading this, you have a certain VO₂ max, a certain strength level, a certain metabolic health, etc. The natural trajectory shows what you’re going to LOSE if you change nothing:

  • 53% of your cardiovascular capacity
  • 50-85% of your strength
  • Your metabolic health (sliding into pre-diabetic/diabetic territory)
  • Your independence (becoming unable to perform basic activities)
  • Decades of vitality, agency, and capability

Behavioural economics research shows we’re 2-3x more motivated to prevent losses than to achieve equivalent gains. So stop thinking about optimisation as “gaining” something. Think about it as refusing to surrender what you currently have.

Every day you don’t train, you’re not just failing to improve. You’re actively giving up the capacity you have today. The trajectory is already in motion. You’re losing ground right now. The question is whether you’re going to fight to keep what’s yours.

Your health is not random. It’s not luck. It’s not purely genetics.

Yes, genetics matter. Yes, some people have advantages or disadvantages built into their DNA. But the trajectories in this calculator make one thing undeniable: your daily choices, compounded over decades, are the large determinants of your health outcomes.

The natural trajectory (the one followed by 70-80% of the population) leads to metabolic disease, cardiovascular disease, sarcopenia, frailty, and loss of independence. This isn’t fear-mongering or exaggeration. This is what the data shows happens when you let modern life run its course without intervention. But the thing that should give you hope is that none of this is inevitable.

The optimisation trajectory shows that you can maintain excellent health markers, physical function, and independence well into your 70s and 80s. You can have the cardiovascular fitness of someone 25-30 years younger. You can maintain strength levels that match or exceed where you were at 30. You can keep your metabolic markers in the optimal range for life. You can prevent the accumulation of arterial damage that leads to heart attacks and strokes.

This isn’t theoretical. This isn’t wishful thinking. This is what happens when you consistently execute the fundamentals: train regularly, eat well, sleep adequately, manage stress, and avoid the obvious toxins like smoking and excessive alcohol.

The question isn’t whether this works. The question is: are you going to do it?

I know what you’re thinking. You’re looking at those optimisation strategies and thinking, “that’s a lot of work.” And you’re right, it is. Training 4-6x/week, tracking nutrition, prioritising 8 hours of sleep, and managing stress proactively, all requires discipline, consistency, and treating your health like a serious priority. But let me reframe this for you: what’s the alternative?

The alternative is the red line on those charts. The alternative is spending your 60s, 70s, and 80s dependent on others, struggling with basic activities, on multiple medications, dealing with chronic disease and pain. The alternative is watching life happen from the sidelines because your body can’t support the activities you want to do.

When you frame it that way, is the optimisation trajectory really that demanding? Is 5 hours a week of training really too much to ask to maintain independence and vitality for decades? Is prioritising sleep really too inconvenient when the payoff is maintaining the metabolic health and physical function to do everything you want to do at 75?

Time is going to pass either way. 

Fifty years from now, you’re going to be 50 years older. The only question is which trajectory will you have followed?

Let me offer you one more frame, this one from the philosopher and mathematician Blaise Pascal. Pascal famously argued for belief in God using what’s now called “Pascal’s Wager”: If God exists and you believe, you gain infinite reward. If God doesn’t exist and you believe, you lose little. If God exists and you don’t believe, you lose infinitely. If God doesn’t exist and you don’t believe, you gain little. The asymmetry makes belief the rational choice.

Apply this to health optimisation:

If you optimise and it works (which all evidence suggests it does):

  • You gain decades of vitality, independence, and capability
  • You maintain agency over your life into your 70s and 80s
  • You avoid years of disease management and decline
  • You remain the protagonist of your own story until the end

If you optimise and somehow it doesn’t work for you specifically:

  • You’ve “lost” 4-5 hours per week training
  • You’ve “sacrificed” some immediate comfort
  • You’ve chosen vegetables over fast food, sleep over late-night TV

If you don’t optimise and the natural trajectory is correct (which it demonstrably is):

  • You lose 50%+ of cardiovascular capacity
  • You lose 50-85% of strength
  • You slide into metabolic disease
  • You lose independence and agency
  • You spend your final decades managing decline

If you don’t optimise, and somehow you’re fine anyway:

  • You’ve gained a few hours per week of leisure time
  • You’ve enjoyed more immediate comfort
  • You’ve eaten whatever you wanted without restriction

Look at that asymmetry. The potential downside of optimisation (a few hours per week of effort) is trivial compared to the potential downside of not optimising (decades of decline, disease, and dependence). The potential upside of optimisation (maintaining vitality and independence for decades) is massive compared to the potential upside of not optimising (a bit more leisure time now).

This isn’t even close. The asymmetry is overwhelming.

Even if you’re sceptical of the exact numbers in the Triage Health Trajectory Tool, even if you think “I might be an outlier”, the asymmetry still holds. The worst case scenario of following the optimisation trajectory is that you end up fit, strong, and healthy for “only” a modest benefit instead of a massive one. The worst case scenario of following the natural trajectory is catastrophic. Choose accordingly.

 

Here’s what I want you to do right now:

  1. Pick one metric where the gap between natural decline and optimisation shocked you. Maybe it was VO₂ max dropping by 53% versus declining by only 16%. Maybe it was HbA1c crossing into diabetic territory versus staying optimal. Maybe it was losing 80% of your chin-up strength versus maintaining it. Whatever metric hit you hardest, that’s your metric to chase.
  2. Make one change this week. Not ten changes. Not a complete life overhaul. One change. Schedule three training sessions for this week. Optimise your protein at each meal. Set a consistent bedtime. Cut out sugary drinks. One change that moves you from the natural trajectory toward the maintenance or optimisation trajectory.
  3. Track one metric. You can’t manage what you don’t measure. If you don’t have recent blood work, schedule it. If you don’t know your VO₂ max, do a fitness test. If you don’t know your body fat percentage, get a DEXA scan. Get a baseline so you can see progress.
  4. Use this tool regularly. Come back to it every 6-12 months. Update your values. See how your trajectory is changing. Let it serve as both a reality check and a source of motivation when you see those numbers improving.
  5. Share this with someone you care about. The people in your life who are following the natural trajectory? They don’t know what you now know. They don’t see the compound effect playing out. They’re making daily decisions without understanding the long-term consequences. Share this tool. Start conversations. Help them see what you now see.

Look, I get it. Reading an article and looking at charts doesn’t automatically change behavior. Knowing what you should do and actually doing it are two different things. If behavior change were easy, everyone would be fit, healthy, and thriving. But what I’ve learned from working with hundreds of clients over the years is that the people who succeed are the ones who truly internalise the compound effect. They understand, at a gut level, that today’s workout isn’t about today, it’s about being able to hike with their grandkids in 30 years. Today’s meal choice isn’t about today, it’s about maintaining optimal metabolic health so they’re not on insulin at 65.

Once you really get that, once you see that your daily choices are votes for which trajectory you’re on, the decisions become easier. Not easy, but easier. Because you’re no longer weighing “should I work out today?” against “I don’t really feel like it.” You’re weighing “30 years on the green line” against “30 years on the red line.” 

The data is clear. The choice is yours. The time to start is now. Not next Monday. Not after the holidays. Not when you’re “less busy.” Now. Because every day you wait is another day on the natural decline trajectory. Another day of arterial damage accumulating. Another day of muscle mass declining. Another day of metabolic health slipping. Another day that compounds into months and years and decades.

Or – every day you take action is another day on the optimization trajectory. Another day of building capacity instead of losing it. Another day of investing in your future health instead of borrowing against it. Fifty years from now, which version of this story do you want to be living? The tools are here. The knowledge is here. The data is here. The only thing missing is your decision to use them.

So what’s it going to be?

The red line, the orange line, or the green line?

Your choice. Your health. Your future.

Make it count.

 

On Mortality and Meaning

One last thing, and then I’ll let you go. The philosopher Martin Heidegger wrote about “being-toward-death”, which is the idea that authentic existence requires acknowledging your own mortality. When you truly internalise that you will die, when you stop treating death as an abstract concept and start seeing it as your concrete, personal, inevitable end, something shifts. Priorities clarify. Trivial concerns fall away. What matters becomes obvious.

These trajectories are a memento mori (a reminder of death). But more specifically, they’re a reminder that your death has a prelude, and that prelude’s quality is largely determined by the choices you’re making right now. You will almost certainly not die suddenly and unexpectedly at 80 while hiking a mountain in perfect health. That’s the fantasy. The reality for most people is a long, slow decline, and years or decades of increasing limitation, dependence, and disease management.

The question isn’t whether you’ll die. The question is what are the ten years before your death going to look like?

On the natural trajectory: probably in and out of hospitals, on multiple medications, struggling with basic activities, dependent on others for care, and your world steadily shrinking as your capabilities diminish.

On the optimisation trajectory: potentially active, independent, engaged with life until the very end, then a relatively quick decline when true biological failure finally arrives.

This is the “compression of morbidity”, which is the compression of the period of disease and disability into as short a period as possible at the very end of life, rather than letting it stretch across decades. That’s what optimisation really is; maintaining the capacity to live fully until you can’t anymore, then dying quickly. Versus slowly surrendering capacity year after year after year, until you’re alive but not really living for the final decade or two of life.

This isn’t about living forever. This is about maintaining human dignity and agency for as long as you’re alive. Most people are familiar with the ancient Roman phrase memento mori (remember you will die), but most people are not familiar with the ancient Roman phrase memento vivere (remember to live). Not just remember you’re going to die, but remember to actually live while you can.

These trajectories are both memento mori and memento vivere. Remember you’re going to die. Remember to actually live until then. The optimisation trajectory is how you do both. That’s it. Close the tab if you want. Or don’t. But if you close it, do so knowing that you’re choosing, and live with that choice consciously.

The trajectories will play out either way. The math doesn’t care about your intentions or your feelings or your circumstances. It just compounds your choices, day after day, year after year, and decade after decade.

If you need more help with your own nutrition, exercise or lifestyle, you can always reach out to us and get online coaching, or alternatively, you can interact with our free content, especially our free nutrition content.

If you want more free information on nutrition or training, you can follow us on Instagram, YouTube or listen to the podcast, where we discuss all the little intricacies of exercise and nutrition. You can always stay up to date with our latest content by subscribing to our newsletter.

Finally, if you want to learn how to coach nutrition, then consider our Nutrition Coach Certification course, and if you want to learn to get better at exercise program design, then consider our course on exercise program design. We do have other courses available too. If you don’t understand something, or you just need clarification, you can always reach out to us on Instagram or via email.

 

References and Further Reading

GENERAL LONGEVITY, MULTI-SYSTEM DECLINE & HALLMARKS OF AGEING

López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. The hallmarks of aging. Cell. 2013;153(6):1194-1217. doi:10.1016/j.cell.2013.05.039 https://pubmed.ncbi.nlm.nih.gov/23746838/

López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. Hallmarks of aging: An expanding universe. Cell. 2023;186(2):243-278. doi:10.1016/j.cell.2022.11.001 https://pubmed.ncbi.nlm.nih.gov/36599349/

Belsky DW, Caspi A, Houts R, et al. Quantification of biological aging in young adults. Proc Natl Acad Sci U S A. 2015;112(30):E4104-E4110. doi:10.1073/pnas.1506264112 https://pubmed.ncbi.nlm.nih.gov/26150497/

Perri G, French C, Agostinis-Sobrinho C, et al. An Expert Consensus Statement on Biomarkers of Aging for Use in Intervention Studies. J Gerontol A Biol Sci Med Sci. 2025;80(5):glae297. doi:10.1093/gerona/glae297 https://pubmed.ncbi.nlm.nih.gov/39708300/

Englund DA, Sakamoto AE, Fritsche CM, et al. Exercise reduces circulating biomarkers of cellular senescence in humans. Aging Cell. 2021;20(7):e13415. doi:10.1111/acel.13415 https://pubmed.ncbi.nlm.nih.gov/34101960/

Moqri M, Herzog C, Poganik JR, et al. Biomarkers of aging for the identification and evaluation of longevity interventions. Cell. 2023;186(18):3758-3775. doi:10.1016/j.cell.2023.08.003 https://pubmed.ncbi.nlm.nih.gov/37657418/

Yusri K, Kumar S, Fong S, Gruber J, Sorrentino V. Towards Healthy Longevity: Comprehensive Insights from Molecular Targets and Biomarkers to Biological Clocks. Int J Mol Sci. 2024;25(12):6793. Published 2024 Jun 20. doi:10.3390/ijms25126793 https://pubmed.ncbi.nlm.nih.gov/38928497/

Cummings SR, Lui LY, Zaira A, et al. Biomarkers of cellular senescence and major health outcomes in older adults. Geroscience. 2025;47(3):3407-3415. doi:10.1007/s11357-024-01474-9 https://pubmed.ncbi.nlm.nih.gov/39695064/

Moqri M, Herzog C, Poganik JR, et al. Validation of biomarkers of aging. Nat Med. 2024;30(2):360-372. doi:10.1038/s41591-023-02784-9 https://pubmed.ncbi.nlm.nih.gov/38355974/

Biomarkers of Aging Consortium, Herzog CMS, Goeminne LJE, et al. Challenges and recommendations for the translation of biomarkers of aging. Nat Aging. 2024;4(10):1372-1383. doi:10.1038/s43587-024-00683-3 https://pubmed.ncbi.nlm.nih.gov/39285015/

 

Trajectories

BLOOD LIPIDS & BLOOD PRESSURE

Song F, Poljak A, Crawford J, et al. Plasma apolipoprotein levels are associated with cognitive status and decline in a community cohort of older individuals. PLoS One. 2012;7(6):e34078. doi:10.1371/journal.pone.0034078 https://pubmed.ncbi.nlm.nih.gov/22701550/

Holme I, Høstmark AT, Anderssen SA. ApoB but not LDL-cholesterol is reduced by exercise training in overweight healthy men. Results from the 1-year randomized Oslo Diet and Exercise Study. J Intern Med. 2007;262(2):235-243. doi:10.1111/j.1365-2796.2007.01806.x https://pubmed.ncbi.nlm.nih.gov/17645591/

Schaefer EJ, Lamon-Fava S, Cohn SD, et al. Effects of age, gender, and menopausal status on plasma low density lipoprotein cholesterol and apolipoprotein B levels in the Framingham Offspring Study. J Lipid Res. 1994;35(5):779-792. https://pubmed.ncbi.nlm.nih.gov/8071601/

Bruno G, Merletti F, Biggeri A, et al. Effect of age on the association of non-high-density-lipoprotein cholesterol and apolipoprotein B with cardiovascular mortality in a Mediterranean population with type 2 diabetes: the Casale Monferrato study. Diabetologia. 2006;49(5):937-944. doi:10.1007/s00125-006-0195-6 https://pubmed.ncbi.nlm.nih.gov/16525840/

Sniderman AD, Islam S, McQueen M, et al. Age and Cardiovascular Risk Attributable to Apolipoprotein B, Low-Density Lipoprotein Cholesterol or Non-High-Density Lipoprotein Cholesterol. J Am Heart Assoc. 2016;5(10):e003665. Published 2016 Oct 13. doi:10.1161/JAHA.116.003665 https://pubmed.ncbi.nlm.nih.gov/27737874/

Walldius G, de Faire U, Alfredsson L, et al. Long-term risk of a major cardiovascular event by apoB, apoA-1, and the apoB/apoA-1 ratio-Experience from the Swedish AMORIS cohort: A cohort study. PLoS Med. 2021;18(12):e1003853. Published 2021 Dec 1. doi:10.1371/journal.pmed.1003853 https://pubmed.ncbi.nlm.nih.gov/34851955/

Jarvik GP, Austin MA, Fabsitz RR, et al. Genetic influences on age-related change in total cholesterol, low density lipoprotein-cholesterol, and triglyceride levels: longitudinal apolipoprotein E genotype effects. Genet Epidemiol. 1994;11(4):375-384. doi:10.1002/gepi.1370110407 https://pubmed.ncbi.nlm.nih.gov/7813899/

Balder JW, de Vries JK, Nolte IM, Lansberg PJ, Kuivenhoven JA, Kamphuisen PW. Lipid and lipoprotein reference values from 133,450 Dutch Lifelines participants: Age- and gender-specific baseline lipid values and percentiles. J Clin Lipidol. 2017;11(4):1055-1064.e6. doi:10.1016/j.jacl.2017.05.007 https://pubmed.ncbi.nlm.nih.gov/28697983/

Rong S, Li B, Chen L, et al. Association of Low-Density Lipoprotein Cholesterol Levels with More than 20-Year Risk of Cardiovascular and All-Cause Mortality in the General Population. J Am Heart Assoc. 2022;11(15):e023690. doi:10.1161/JAHA.121.023690 https://pubmed.ncbi.nlm.nih.gov/35904192/

Postmus I, Deelen J, Sedaghat S, et al. LDL cholesterol still a problem in old age? A Mendelian randomization study. Int J Epidemiol. 2015;44(2):604-612. doi:10.1093/ije/dyv031 https://pubmed.ncbi.nlm.nih.gov/25855712/

Zhang Y, Woo JG, Urbina EM, Jacobs DR Jr, Moran AE, de Ferranti SD. Low-Density Lipoprotein Cholesterol Trajectories and Prevalence of High Low-Density Lipoprotein Cholesterol Consistent With Heterozygous Familial Hypercholesterolemia in US Children. JAMA Pediatr. 2021;175(10):1071-1074. doi:10.1001/jamapediatrics.2021.2046 https://pubmed.ncbi.nlm.nih.gov/34279542/

Jarvik GP, Goode EL, Austin MA, et al. Evidence that the apolipoprotein E-genotype effects on lipid levels can change with age in males: a longitudinal analysis. Am J Hum Genet. 1997;61(1):171-181. doi:10.1086/513902 https://pubmed.ncbi.nlm.nih.gov/9245998/

Spitler KM, Davies BSJ. Aging and plasma triglyceride metabolism. J Lipid Res. 2020;61(8):1161-1167. doi:10.1194/jlr.R120000922 https://pubmed.ncbi.nlm.nih.gov/32586846/

Greenfield MS, Kraemer F, Tobey T, Reaven G. Effect of age on plasma triglyceride concentrations in man. Metabolism. 1980;29(11):1095-1099. doi:10.1016/0026-0495(80)90221-8 https://pubmed.ncbi.nlm.nih.gov/7001176/

Zhou Z, Ryan J, Tonkin AM, et al. Association Between Triglycerides and Risk of Dementia in Community-Dwelling Older Adults: A Prospective Cohort Study. Neurology. 2023;101(22):e2288-e2299. Published 2023 Nov 27. doi:10.1212/WNL.0000000000207923 https://pubmed.ncbi.nlm.nih.gov/37879942/

Dayimu A, Wang C, Li J, et al. Trajectories of Lipids Profile and Incident Cardiovascular Disease Risk: A Longitudinal Cohort Study. J Am Heart Assoc. 2019;8(21):e013479. doi:10.1161/JAHA.119.013479 https://pubmed.ncbi.nlm.nih.gov/31630587/

Abbott RD, Sharp DS, Burchfiel CM, et al. Cross-sectional and longitudinal changes in total and high-density-lipoprotein cholesterol levels over a 20-year period in elderly men: the Honolulu Heart Program. Ann Epidemiol. 1997;7(6):417-424. doi:10.1016/s1047-2797(97)00043-4 https://pubmed.ncbi.nlm.nih.gov/9279451/

Weijenberg MP, Feskens EJ, Kromhout D. Age-related changes in total and high-density-lipoprotein cholesterol in elderly Dutch men. Am J Public Health. 1996;86(6):798-803. doi:10.2105/ajph.86.6.798 https://pubmed.ncbi.nlm.nih.gov/8659652/

Wilson PW, Anderson KM, Harris T, Kannel WB, Castelli WP. Determinants of change in total cholesterol and HDL-C with age: the Framingham Study. J Gerontol. 1994;49(6):M252-M257. doi:10.1093/geronj/49.6.m252 https://pubmed.ncbi.nlm.nih.gov/7963277/

Harman JL, Griswold ME, Jeffries NO, et al. Age is positively associated with high-density lipoprotein cholesterol among African Americans in cross-sectional analysis: the Jackson Heart Study. J Clin Lipidol. 2011;5(3):173-178. doi:10.1016/j.jacl.2011.02.002 https://pubmed.ncbi.nlm.nih.gov/21600522/

Landahl S, Bengtsson C, Sigurdsson JA, Svanborg A, Svärdsudd K. Age-related changes in blood pressure. Hypertension. 1986;8(11):1044-1049. doi:10.1161/01.hyp.8.11.1044 https://pubmed.ncbi.nlm.nih.gov/3770866/

Pearson JD, Morrell CH, Brant LJ, Landis PK, Fleg JL. Age-associated changes in blood pressure in a longitudinal study of healthy men and women. J Gerontol A Biol Sci Med Sci. 1997;52(3):M177-M183. doi:10.1093/gerona/52a.3.m177 https://pubmed.ncbi.nlm.nih.gov/9158560/

Franklin SS, Gustin W 4th, Wong ND, et al. Hemodynamic patterns of age-related changes in blood pressure. The Framingham Heart Study. Circulation. 1997;96(1):308-315. doi:10.1161/01.cir.96.1.308 https://pubmed.ncbi.nlm.nih.gov/9236450/

 

METABOLIC MARKERS (Fasting Glucose & HbA1c)

Dubowitz N, Xue W, Long Q, et al. Aging is associated with increased HbA1c levels, independently of glucose levels and insulin resistance, and also with decreased HbA1c diagnostic specificity. Diabet Med. 2014;31(8):927-935. doi:10.1111/dme.12459 https://pubmed.ncbi.nlm.nih.gov/24698119/

Bremner AP, Feddema P, Leedman PJ, et al. Age-related changes in thyroid function: a longitudinal study of a community-based cohort. J Clin Endocrinol Metab. 2012;97(5):1554-1562. doi:10.1210/jc.2011-3020 https://pubmed.ncbi.nlm.nih.gov/22344200/

Yates AP, Laing I. Age-related increase in haemoglobin A1c and fasting plasma glucose is accompanied by a decrease in beta cell function without change in insulin sensitivity: evidence from a cross-sectional study of hospital personnel. Diabet Med. 2002;19(3):254-258. doi:10.1046/j.1464-5491.2002.00644.x https://pubmed.ncbi.nlm.nih.gov/11918628/

Heianza Y, Arase Y, Fujihara K, et al. Longitudinal trajectories of HbA1c and fasting plasma glucose levels during the development of type 2 diabetes: the Toranomon Hospital Health Management Center Study 7 (TOPICS 7). Diabetes Care. 2012;35(5):1050-1052. doi:10.2337/dc11-1793 https://pubmed.ncbi.nlm.nih.gov/22456865/

Yu HJ, Ho M, Chau PH, Fong DYT. Trajectories of fasting glucose and glycated haemoglobin in obese and non-obese incident diabetes: Results from two large cohort studies. Diabetes Obes Metab. 2023;25(10):2835-2845. doi:10.1111/dom.15173 https://pubmed.ncbi.nlm.nih.gov/37336785/

Heianza Y, Hara S, Arase Y, et al. HbA1c 5·7-6·4% and impaired fasting plasma glucose for diagnosis of prediabetes and risk of progression to diabetes in Japan (TOPICS 3): a longitudinal cohort study. Lancet. 2011;378(9786):147-155. doi:10.1016/S0140-6736(11)60472-8 https://pubmed.ncbi.nlm.nih.gov/21705064/

Zheng F, Yan L, Yang Z, Zhong B, Xie W. HbA1c, diabetes and cognitive decline: the English Longitudinal Study of Ageing. Diabetologia. 2018;61(4):839-848. doi:10.1007/s00125-017-4541-7 https://pubmed.ncbi.nlm.nih.gov/29368156/

Yu J, Sun H, Shang F, et al. Association Between Glucose Metabolism And Vascular Aging In Chinese Adults: A Cross-Sectional Analysis In The Tianning Cohort Study. Clin Interv Aging. 2019;14:1937-1946. Published 2019 Nov 6. doi:10.2147/CIA.S223690 https://pubmed.ncbi.nlm.nih.gov/31806949/

Lipska KJ, Inzucchi SE, Van Ness PH, et al. Elevated HbA1c and fasting plasma glucose in predicting diabetes incidence among older adults: are two better than one?. Diabetes Care. 2013;36(12):3923-3929. doi:10.2337/dc12-2631 https://pubmed.ncbi.nlm.nih.gov/24135387/

Fatih N, Hughes A, Sudre CH, et al. Sex differences between mid-life glycaemic traits and brain volume at age 70: a population-based study. Eur J Endocrinol. 2025;192(5):K44-K49. doi:10.1093/ejendo/lvaf090 https://pubmed.ncbi.nlm.nih.gov/40300998/

Jung JY, Ryoo JH, Chung PW, Oh CM, Choi JM, Park SK. Association of fasting glucose and glycated hemoglobin with the long-term risk of incident metabolic syndrome: Korean Genome and Epidemiology Study (KoGES). Acta Diabetol. 2019;56(5):551-559. doi:10.1007/s00592-019-01290-0 https://pubmed.ncbi.nlm.nih.gov/30900026/

Lindeman RD, Yau CL, Baumgartner RN, Morley JE, Garry PJ; New Mexico Aging Process Study. Longitudinal study of fasting serum glucose concentrations in healthy elderly. The New Mexico Aging Process Study. J Nutr Health Aging. 2003;7(3):172-177. https://pubmed.ncbi.nlm.nih.gov/12766795/

 

INFLAMMATION & IMMUNE (hs-CRP & WBC)

Laurin D, David Curb J, Masaki KH, White LR, Launer LJ. Midlife C-reactive protein and risk of cognitive decline: a 31-year follow-up. Neurobiol Aging. 2009;30(11):1724-1727. doi:10.1016/j.neurobiolaging.2008.01.008 https://pubmed.ncbi.nlm.nih.gov/18316138/

McGwin G, Hall TA, Xie A, Owsley C. The relation between C reactive protein and age related macular degeneration in the Cardiovascular Health Study. Br J Ophthalmol. 2005;89(9):1166-1170. doi:10.1136/bjo.2005.067397 https://pubmed.ncbi.nlm.nih.gov/16113374/

Ruggiero C, Metter EJ, Cherubini A, et al. White blood cell count and mortality in the Baltimore Longitudinal Study of Aging. J Am Coll Cardiol. 2007;49(18):1841-1850. doi:10.1016/j.jacc.2007.01.076 https://pubmed.ncbi.nlm.nih.gov/17481443/

Verschoor CP, Vlasschaert C, Rauh MJ, Paré G. A DNA methylation based measure outperforms circulating CRP as a marker of chronic inflammation and partly reflects the monocytic response to long-term inflammatory exposure: A Canadian Longitudinal Study on Aging analysis. Aging Cell. 2023;22(7):e13863. doi:10.1111/acel.13863 https://pubmed.ncbi.nlm.nih.gov/37139638/

Goto M, Sugimoto K, Hayashi S, et al. Aging-associated inflammation in healthy Japanese individuals and patients with Werner syndrome. Exp Gerontol. 2012;47(12):936-939. doi:10.1016/j.exger.2012.08.010 https://pubmed.ncbi.nlm.nih.gov/22960593/

Lassale C, Batty GD, Steptoe A, et al. Association of 10-Year C-Reactive Protein Trajectories With Markers of Healthy Aging: Findings From the English Longitudinal Study of Aging. J Gerontol A Biol Sci Med Sci. 2019;74(2):195-203. doi:10.1093/gerona/gly028 https://pubmed.ncbi.nlm.nih.gov/29462285/

Samson LD, Boots AMH, Verschuren WMM, Picavet HSJ, Engelfriet P, Buisman AM. Frailty is associated with elevated CRP trajectories and higher numbers of neutrophils and monocytes. Exp Gerontol. 2019;125:110674. doi:10.1016/j.exger.2019.110674 https://pubmed.ncbi.nlm.nih.gov/31336145/

Chen C, Liu Y, Cao Z, et al. Combined associations of hs-CRP and cognitive function with all-cause mortality among oldest-old adults in Chinese longevity areas: a prospective cohort study. Immun Ageing. 2019;16:30. Published 2019 Nov 17. doi:10.1186/s12979-019-0170-y https://pubmed.ncbi.nlm.nih.gov/31832073/

Caldeira MHR, Mello Almada-Filho C, Brunialti MKC, Salomão R, Cendoroglo M. Immune Profile and Body Composition of Independent Oldest Old: The Longevous Project. Gerontology. 2023;69(6):660-670. doi:10.1159/000527485 https://pubmed.ncbi.nlm.nih.gov/36657402/

Zhai Y, Shi XM, Fitzgerald SM, et al. High sensitivity C-reactive protein associated with different health predictors in middle-aged and oldest old Chinese. Biomed Environ Sci. 2012;25(3):257-266. doi:10.3967/0895-3988.2012.03.002 https://pubmed.ncbi.nlm.nih.gov/22840575/

 

LIVER, KIDNEY & THYROID

Schmucker DL. Age-related changes in liver structure and function: Implications for disease ?. Exp Gerontol. 2005;40(8-9):650-659. doi:10.1016/j.exger.2005.06.009 https://pubmed.ncbi.nlm.nih.gov/16102930/

Malmgren L, McGuigan FE, Berglundh S, Westman K, Christensson A, Åkesson K. Declining Estimated Glomerular Filtration Rate and Its Association with Mortality and Comorbidity Over 10 Years in Elderly Women. Nephron. 2015;130(4):245-255. doi:10.1159/000435790 https://pubmed.ncbi.nlm.nih.gov/26184510/

Cohen E, Nardi Y, Krause I, et al. A longitudinal assessment of the natural rate of decline in renal function with age. J Nephrol. 2014;27(6):635-641. doi:10.1007/s40620-014-0077-9 https://pubmed.ncbi.nlm.nih.gov/24643437/

Baba M, Shimbo T, Horio M, et al. Longitudinal Study of the Decline in Renal Function in Healthy Subjects. PLoS One. 2015;10(6):e0129036. Published 2015 Jun 10. doi:10.1371/journal.pone.0129036 https://pubmed.ncbi.nlm.nih.gov/26061083/

Gorski M, Rasheed H, Teumer A, et al. Genetic loci and prioritization of genes for kidney function decline derived from a meta-analysis of 62 longitudinal genome-wide association studies. Kidney Int. 2022;102(3):624-639. doi:10.1016/j.kint.2022.05.021 https://pubmed.ncbi.nlm.nih.gov/35716955/

Guppy M, Thomas ET, Glasziou P, et al. Rate of decline in kidney function with age: a systematic review. BMJ Open. 2024;14(11):e089783. Published 2024 Nov 27. doi:10.1136/bmjopen-2024-089783 https://pubmed.ncbi.nlm.nih.gov/39609029/

Jiang S, Sun X, Gu H, et al. Age-related change in kidney function, its influencing factors, and association with asymptomatic carotid atherosclerosis in healthy individuals–a 5-year follow-up study. Maturitas. 2012;73(3):230-238. doi:10.1016/j.maturitas.2012.07.014 https://pubmed.ncbi.nlm.nih.gov/22951150/

van der Burgh AC, Rizopoulos D, Ikram MA, Hoorn EJ, Chaker L. Determinants of the Evolution of Kidney Function With Age. Kidney Int Rep. 2021;6(12):3054-3063. Published 2021 Oct 16. doi:10.1016/j.ekir.2021.10.006 https://pubmed.ncbi.nlm.nih.gov/34901574/

Bremner AP, Feddema P, Leedman PJ, et al. Age-related changes in thyroid function: a longitudinal study of a community-based cohort. J Clin Endocrinol Metab. 2012;97(5):1554-1562. doi:10.1210/jc.2011-3020 https://pubmed.ncbi.nlm.nih.gov/22344200/

Waring AC, Arnold AM, Newman AB, Bùzková P, Hirsch C, Cappola AR. Longitudinal changes in thyroid function in the oldest old and survival: the cardiovascular health study all-stars study. J Clin Endocrinol Metab. 2012;97(11):3944-3950. doi:10.1210/jc.2012-2481 https://pubmed.ncbi.nlm.nih.gov/22879629/

Lipson A, Nickoloff EL, Hsu TH, et al. A study of age-dependent changes in thyroid function tests in adults. J Nucl Med. 1979;20(11):1124-1130. https://pubmed.ncbi.nlm.nih.gov/536771/

 

CARDIOVASCULAR FITNESS (VO₂max, RHR, HRV)

Fleg JL, Lakatta EG. Role of muscle loss in the age-associated reduction in VO2 max. J Appl Physiol (1985). 1988;65(3):1147-1151. doi:10.1152/jappl.1988.65.3.1147 https://pubmed.ncbi.nlm.nih.gov/3182484/

Rogers MA, Hagberg JM, Martin WH 3rd, Ehsani AA, Holloszy JO. Decline in VO2max with aging in master athletes and sedentary men. J Appl Physiol (1985). 1990;68(5):2195-2199. doi:10.1152/jappl.1990.68.5.2195 https://pubmed.ncbi.nlm.nih.gov/2361923/

Hawkins S, Wiswell R. Rate and mechanism of maximal oxygen consumption decline with aging: implications for exercise training. Sports Med. 2003;33(12):877-888. doi:10.2165/00007256-200333120-00002 https://pubmed.ncbi.nlm.nih.gov/12974656/

Marks RG, Hale WE, Moore MT, May FE, Stewart RB. Resting heart rates in an ambulatory elderly population: an evaluation of age, sex, symptoms, and medication. Gerontology. 1989;35(4):210-217. doi:10.1159/000213025 https://pubmed.ncbi.nlm.nih.gov/2511084/

Umetani K, Singer DH, McCraty R, Atkinson M. Twenty-four hour time domain heart rate variability and heart rate: relations to age and gender over nine decades. J Am Coll Cardiol. 1998;31(3):593-601. doi:10.1016/s0735-1097(97)00554-8 https://pubmed.ncbi.nlm.nih.gov/9502641/

Hawkins SA, Marcell TJ, Victoria Jaque S, Wiswell RA. A longitudinal assessment of change in VO2max and maximal heart rate in master athletes. Med Sci Sports Exerc. 2001;33(10):1744-1750. doi:10.1097/00005768-200110000-00020 https://pubmed.ncbi.nlm.nih.gov/11581561/

Burtscher J, Strasser B, Burtscher M, Millet GP. The Impact of Training on the Loss of Cardiorespiratory Fitness in Aging Masters Endurance Athletes. Int J Environ Res Public Health. 2022;19(17):11050. Published 2022 Sep 3. doi:10.3390/ijerph191711050 https://pubmed.ncbi.nlm.nih.gov/36078762/

Wendell CR, Gunstad J, Waldstein SR, Wright JG, Ferrucci L, Zonderman AB. Cardiorespiratory fitness and accelerated cognitive decline with aging. J Gerontol A Biol Sci Med Sci. 2014;69(4):455-462. doi:10.1093/gerona/glt144 https://pubmed.ncbi.nlm.nih.gov/24192540/

 

STRENGTH & BODY COMPOSITION

Mitchell WK, Williams J, Atherton P, Larvin M, Lund J, Narici M. Sarcopenia, dynapenia, and the impact of advancing age on human skeletal muscle size and strength; a quantitative review. Front Physiol. 2012;3:260. Published 2012 Jul 11. doi:10.3389/fphys.2012.00260 https://pubmed.ncbi.nlm.nih.gov/22934016/

Jackson AS, Janssen I, Sui X, Church TS, Blair SN. Longitudinal changes in body composition associated with healthy ageing: men, aged 20-96 years. Br J Nutr. 2012;107(7):1085-1091. doi:10.1017/S0007114511003886 https://pubmed.ncbi.nlm.nih.gov/21810289/

Shen Y, Shi Q, Nong K, et al. Exercise for sarcopenia in older people: A systematic review and network meta-analysis. J Cachexia Sarcopenia Muscle. 2023;14(3):1199-1211. doi:10.1002/jcsm.13225 https://pubmed.ncbi.nlm.nih.gov/37057640/

Beaudart C, Zaaria M, Pasleau F, Reginster JY, Bruyère O. Health Outcomes of Sarcopenia: A Systematic Review and Meta-Analysis. PLoS One. 2017;12(1):e0169548. Published 2017 Jan 17. doi:10.1371/journal.pone.0169548 https://pubmed.ncbi.nlm.nih.gov/28095426/

Petermann-Rocha F, Balntzi V, Gray SR, et al. Global prevalence of sarcopenia and severe sarcopenia: a systematic review and meta-analysis. J Cachexia Sarcopenia Muscle. 2022;13(1):86-99. doi:10.1002/jcsm.12783 https://pubmed.ncbi.nlm.nih.gov/34816624/

Peng TC, Chen WL, Wu LW, Chang YW, Kao TW. Sarcopenia and cognitive impairment: A systematic review and meta-analysis. Clin Nutr. 2020;39(9):2695-2701. doi:10.1016/j.clnu.2019.12.014 https://pubmed.ncbi.nlm.nih.gov/31917049/

 

RECOVERY & HORMONES (Sleep & Testosterone)

Miller MA, Wright H, Ji C, Cappuccio FP. Cross-sectional study of sleep quantity and quality and amnestic and non-amnestic cognitive function in an ageing population: the English Longitudinal Study of Ageing (ELSA). PLoS One. 2014;9(6):e100991. Published 2014 Jun 26. doi:10.1371/journal.pone.0100991 https://pubmed.ncbi.nlm.nih.gov/24968354/

Harman SM, Metter EJ, Tobin JD, Pearson J, Blackman MR; Baltimore Longitudinal Study of Aging. Longitudinal effects of aging on serum total and free testosterone levels in healthy men. Baltimore Longitudinal Study of Aging. J Clin Endocrinol Metab. 2001;86(2):724-731. doi:10.1210/jcem.86.2.7219 https://pubmed.ncbi.nlm.nih.gov/11158037/

Feldman HA, Longcope C, Derby CA, et al. Age trends in the level of serum testosterone and other hormones in middle-aged men: longitudinal results from the Massachusetts male aging study. J Clin Endocrinol Metab. 2002;87(2):589-598. doi:10.1210/jcem.87.2.8201 https://pubmed.ncbi.nlm.nih.gov/11836290/

Matthews KA, Kravitz HM, Lee L, et al. Does midlife aging impact women’s sleep duration, continuity, and timing?: A longitudinal analysis from the Study of Women’s Health Across the Nation. Sleep. 2020;43(4):zsz259. doi:10.1093/sleep/zsz259 https://pubmed.ncbi.nlm.nih.gov/31633180/

Didikoglu A, Maharani A, Tampubolon G, Canal MM, Payton A, Pendleton N. Longitudinal sleep efficiency in the elderly and its association with health. J Sleep Res. 2020;29(3):e12898. doi:10.1111/jsr.12898 https://pubmed.ncbi.nlm.nih.gov/31313420/

Åkerstedt T, Discacciati A, Miley-Åkerstedt A, Westerlund H. Aging and the Change in Fatigue and Sleep – A Longitudinal Study Across 8 Years in Three Age Groups. Front Psychol. 2018;9:234. Published 2018 Mar 8. doi:10.3389/fpsyg.2018.00234 https://pubmed.ncbi.nlm.nih.gov/29568279/

Hublin C, Haasio L, Kaprio J. Changes in self-reported sleep duration with age – a 36-year longitudinal study of Finnish adults. BMC Public Health. 2020;20(1):1373. Published 2020 Sep 9. doi:10.1186/s12889-020-09376-z https://pubmed.ncbi.nlm.nih.gov/32907578/

 

Author

  • Paddy Farrell

    Hey, I'm Paddy!

    I am a coach who loves to help people master their health and fitness. I am a personal trainer, strength and conditioning coach, and I have a degree in Biochemistry and Biomolecular Science. I have been coaching people for over 10 years now.

    When I grew up, you couldn't find great health and fitness information, and you still can't really. So my content aims to solve that!

    I enjoy training in the gym, doing martial arts, hiking in the mountains (around Europe, mainly), drawing and coding. I am also an avid reader of philosophy, history, and science. When I am not in the mountains, exercising or reading, you will likely find me in a museum.

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